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SUBJECT SEMINAR
APPROACH TO SPINAL CORD LESIONS
GUIDE- Dr KALINGA B Sir
STUDENT- Dr SATISH PATIL
DEFINITION
Insult to spinal cord resulting in change in the
normal motor,sensory or autonomic function. This
change either temporary or permanent.
ANATOMY
Spinal cord lies within protective covering of vertebral column.
Begins just below foramen magnum of skull
Ends opposite 2nd lumbar vertebra
Below L2 continue as leash of nerve roots known as cauda equina.
Prolongation of Pia matter forms Filum terminale
Relation of spinal nerve roots to vertebrae
Spinal cord level Corresponding vertebral body
Upper cervical Same as cord level
Lower cervical One level higher
Upper thoracic Two levels higher
Lower thoracic 2 – 3 levels higher
Lumbar T10 – T12
Sacral T12 – L1
Markers for sensory level
T4 Nipple
T10 Umbilicus
T12 Pubic symphysis
Conus medullaris
• Conical structure
• Continuous with filum terminale
Cauda equina
• Sheath of nerve root from lumbar and
caudal segments in subarachnoid
space enlargement.
• Horse tail appearance
Filum terminale
• 20 cm long
• Below the level of conus medullaris
only piamater is continued as a
fibrous cord.
Reflex arc
 Involuntary response to a stimulus.
 Where sensory and motor nerves arise from cord
Sensory fibers enter posterior
Synapse in the grey matter
Motor fibers leave anterior
Spinal cord – blood supply
• Anterior spinal artery
Supplies ventral 2/3 of SC (anterior and lateral column)
One in number
• Posterior spinal artery
Supplies dorsal 1/3 of SC (posterior column)
Two in number
Radicular arteries
Upper half of cervical cord- no
Lower cervical & first two thoracic- 4
Mid thoracic- 1
Lower thoracic to coccygeal- arterial radicularis magna
Myelopathy – approach
Symptoms
• Limb weakness
• Loss of pain and temperature
• Loss of joint, position and vibration
• Sharp shooting back pain (aggravated by cough)
• Bowel and bladder incontinence
Approach to patient
History
Onset
1.Sudden – trauma – Fracture dislocation of vertebrae
infection – Epidural abscess
vascular- Thrombosis of ASA , hematomyelia ,
Transverse myelitis , multiple sclerosis
2.Gradual – Neoplastic – meningioma , ependymoma , glioma,
astrocytoma
Sensory: 1.sacral sparing - intramedullary lesion)
2.radicular(root) pain- extramedullary lesion
3.poorly localised burning pain- intramedullary lesion
Motor –limb involvement symmetrical or sequential
-weakness more in proximal muscles ( difficulty in getting from
sitting posture , climbing stairs , buckling of knees)
- weakness is progressive or static
H/O diurnal variation of weakness or fatiguability suggests – NMD(myesthenia
gravis)
H/O presence of stiffness or scissoring of limbs while walking, involuntary
movements ( flexor spasms –UMN lesion)
Sphincter disturbances
- urgency,hesitancy – UMN type of bladder
- Painful retention with overflow incontinence – LMN etiology
- Early bladder involvement – intramedullary lesion
Associated symptoms
 Fever – infective causes
 Seizures, delayed milestones
 Associated specific symptoms – vit B12 deficiency
History about
 Preceding illness
 Trauma
 Prior vaccination
Examination
General physical examination
o Lymph node ( TB, lymphoma, malignancy)
o Temperature ( TB, acute transverse myelitis)
o Skin ( café au lait spots in neurofibroma, trophic changes)
Higher mental function
o Affected in cerebral and degenerative diseases
o Staccato speech in multiple sclerosis
o Dysarthria in ALS and syringomyelia
Cranial nerve examination
• Affected in brain stem lesions
• Optic atrophy – friedrich ataxia , multiple sclerosis
• Nystagmus in multiple sclerosis
• Pupillary changes in neurosyphilis
• Difficulty on swallowing – ALS
Tone and DTR
• Increased in UMN
• Decreased in LMN
Sensory examination
Proper examination of skull and spine
Paraplegia
• Pyramidal (UMN ) lesion – spastic paraplegia
• Lower motor neuron ( LMN ) lesion – flaccid paraplegia
Spastic paraplegia
• Weakness of muscle along with increased tone
• Occurs due to UMN disease
Increased tone
Exagerated DTR
Plantar extension
Further devided;
-Paraplegia in extension
-Paraplegia in flexion
Paraplegia in extension Paraplegia in flexion
Cause Pyramidal lesion Pyramidal or extrapyramidal
Hypertonia More in extensors More in flexors
Position of LL Extended Flexed
Deep reflexes Exaggerated Less exagerated
Clonus Present Absent
Mass reflex Absent May be present
Bladder precipitancy Autonomic bladder
Causes
Cortical
Superior saggital sinus thrombosis
Thrombosis of unpaired anterior cerebral artery
Parasaggital meningioma
Multiple sclerosis
Space occupying lesion over motor area ; gliomas
Myelopathy – classification
Myelopathy
Compressive Non compressive
Extradural Intradural
Extramedullary Intramedullary
Compressive myelopathy
1.Extradural
Craniovertebral anomalies
Cervical spondylosis
Trauma
Epidural abscess
Aortic aneurysm compressing vertebral column
Myeloma
metastasis
2.Intradural
Extramedullary lesion Intramedullary lesion
Manifestations Stage 1: Root pain
Stage 2: brown Sequard syndrome
Stage 3: complete transection
Motor UMN- early involvement with sacral sparing
LMN- not involved
UMN- late involvement
LMN- due to AHC affection
Sensory Dissociative sensory loss
(spinothalamic lost, posterior column
spared)
ANS Not very common Early bowel and bladder involvement
Trophic changes Not very common Common due to loss of pain
Spinal deformity
Spinal tenderness
Present Absent
CSF proteins Present Absent
Examples Trauma
Tumour/mets
Aneurysm
TB/ syphilis
Neurofibroma
Meningioma
Arachnoid cyst
Pachymeningitis
Tumors
• Most spinal tumors are extradural – about 85%
Primary- spine
Secondary – lung, breast,prostate,kidney ,thyroid
Symptoms
-pain
-numbness
-muscle weakness ,spasticity
-loss of bowel and bladder control
1.Extradural tumors
 Most common spinal tumor -85%
 Mostly metastatic
 Arise from osseous element
of spinal column.
 Primary: lung,breast,
prostate and kidney.
 Collapse of vertebrae distortion
and narrowing.
Ex ;
1. -Lymphoma
2. -Hemangioma
3. -Neuroblastoma
2.Intradural extramedullary tumors
• Inside the dura but outside the spinal cord.
• Arise from dural sheath around the cord or shwann
cell sheath around the spinal root
• Can grow into retroperitoneal or retropleural through
intervertebral foramen
Ex;
Meningeoma
Neurinoma
3.Intradural intramedullary tumors
• Inside the spinal cord
• Arise from glial elements
of spinal cord
• More common in children
Ex
Astrocytoma –most common
intramedullary tumor of childhood.
Ependymoma – most common
intramedullary tumor of adulthood
Non compressive myelopthies
1. Infections: TB/ HIV/ Lyme’s disease
2. Demyelinating disorders: Multiple sclerosis, ATM
3. Nutritional: SACD
4. Vascular: Anterior spinal artery syndrome, Leriche’s syndrome
5. Autoimmune: Lupus
6. Traumatic: Electric shock
7. Hereditary: Freidrich’s ataxia
8. Toxic: Lathyrism, flourosis
Pott’s disease
Infection reaches – Hematogenous spread
- Adjescent paravertebral lymph nodes
Involves two or more vertebral bodies
Most common – lower thoracic and upper lumbar vertebra
Collapsed vertebra or abscess cause compression of spinal cord leading to
paraparesis
X-ray shows decreased vertebral height collapsed vertebrae and irregular
vertebral margins
Acute transverse
myelitis
Gullian barre
syndrome
Lower limb > upper
limb
Progressive lower limb
Proximal>distal
Weakness Symmetrical Ascends to upper
limbs and to face
Sensory Sensory ataxia Normal
Reflexes Hyperreflexia below
the lesion
Areflexia
Bladder symptoms + -
Band like sensation
(Definite sensory level)
-
Friedreich’s ataxia and Sub acute combined degeneration
FRIEDREICH’S ATAXIA SACD
DRG -> Spinal cord ->
Peripheral nerves
Post column -> CST ->
Peripheral neuropathy
Reflexes Areflexia in lower limb Lost due to peripheral
neuropathy
Sensory Sensory ataxia Loss of vibration sense
Tingling and numbness
Weakness UMN type UMN type
Associated
findings
Cardiomyopathy
Optic atrophy
Vitamin B12 deficiency
Bilateral optic neuropathy
Dementia
Quadripares /quadriplegia
Compressive
1.Trauma
2.Tumors
- Metastatic
- Primary
3.Vertebral disease
-Disc Prolapse
-Spondylosis
-Pagets Disease
-Deformity
Non compressive
• Infection – bacterial osteomyelitis, spinal abscess, HIV infection
• Inflammatory – transverse myelitis, multiple sclerosis, SLE.
• Vascular – Anterior spinal artery occlusion
-Angioma
-Av malformation
• Others
-Degenerative MND
-Vit B12 deficiency
Spinal cord injury
1.Primary
- initial mechanism of injury
2. Secondary
Ongoing progressive damage
- Ischemia
- Hypoxia
- Microhemorrhage
- Edema
Statistics
National Spinal Cord Injury Database ( NSCISC)
 MVA - 38.2%%
Falls - 32.3%
Violence - 14.3%
Sports - 7.8%
Medical and surgical- 4.1%
-55% cases occur in 16- 30 years of age
- Among 81.6% are male.
Mechanism of injury
 Flexion
 Hyperflexion
 Compression
 Rotation
Flexion (hyper flexion)
• Most common because of natural protection position
Compression
• Cause by force from above , as hit on head
• Below as landing on butt
• Usually affects lumbar region
Rotation
• Most unstable
• Results in tearing of ligamentous structures that normally stabilize the
spine
• Usually results in serious neurologic deficits.
Classification of spinal cord injury
(Degree of injury )
1. Complete
2. Incomplete
 Central cord syndrome
 Anterior cord syndrome
 Brown sequard syndrome
 Posterior cord syndrome
 Cauda equina and conus medullaris
Complete
Features
- Loss of voluntary movement
of parts innervated by segment
this is irreversible.
- Spinal shock
Deficits
 Motor – spastic paralysis below level of injury
 Sensory – loss of all sensation perception
 Autonomic – vasomotor failure and spastic bladder
Incomplete
 Some function is present below site of injury
 More favourable prognosis overall
 Are recognizable pattern of injury, although they are rarely pure and
variations occur
Central cord syndrome
 Injury to center of the cord
by edema and hemorrhage
 Motor weakness and sensory loss in all extremities
 Upper extremities affected more
Anterior cord syndrome
 Injury to anterior cord
 Loss of voluntary motor,
pain and temperature perception below injury
 Retains posterior column function
(sensation of touch , position, vibration, motion)
Posterior cord syndrome
 Least frequent syndrome
 Injury to the posterior(dorsal) column
 Loss of proprioception, pain , temperature sensation.
 Motor function below the
level of lesion remain intact
 Usually good power and sensation
Brown – Sequard syndrome:
 Hemisection of cord
 Ipsilateral paralysis
 Ipsilateral superficial sensation,
vibration and proprioception loss.
 Contralateral loss of pain and
temperature perception.
Cauda equina and conus medullaris
Conus medullaris
- injury to the sacral cord (conus) and lumbar
nerve roots
Cauda equina
- injury to the lumbosacral nerve roots
RESULT - areflexic ( flaccid) bladder and bowel , flaccid lower limbs
Conus medullaris and cauda equina syndrome
Conus medullaris syndrome Cauda equina syndrome
Vertebral level L1-L2 L2-sacram
Spinal level Sacral cord segment and roots Lumbosacral nerve roots
Presentation Sudden and bilateral Gradual and unilateral
Radicular pain Less severe More severe
Low back pain More Less
Motor strength Symmetrical,less marked hyperreflexic distal
paresis of lower limb, fasciculation
Symmetric , more marked ,areflexic
paraplegia, atrophy more common
Reflexes Ankle jerks affected Both knee and anke jerks affected
Sensory Localised numbness to perianal
area,symmetrical and bilateral
Localised numbness at saddle area,
asymmetrical,unilateral
Sphincter dysfunction Early urinary and fecal incontinence Tend to present late
Syringomyelia
Cavitatory expansion of central canal of spinal cord (lower cervical)
Associated with ARNOLD CHIARI MALFORMATION TYPE 1 (75%)
Syringomyelia reaching medulla is syringobulbia
Clinical features
• Like an intramedullary lesion
• HALF CAPE distribution of sensory loss
Sensory loss along chest, upper arm, shoulder
• ONION PEEL PATTERN ON FACE
Loss of sensation on face
• Compression of AHC
Wasting of thenar eminence, forearm, arm
• Spastic weakness
• Horner’s syndrome (C8-T1)
Chiari malformation
Type 1 Herniation of cerebellear
tonsils
Associated with
syringomyelia
Type 2 (Arnold Chiari) Herniation of cerebellar
vermis
Usually accompanies by a
lumbar myelomeningocele
Type 3 Occipital encephalocele Usually with
syringomyelia,tethered
cord and hydrocephalous
Type 4 Lack of cerebellar
development
Not compatible with life
Clinical manifestations based on the level of the lesion
1) Lesion at foramen magnum
• Around the clock weakness or ELSBERG PHENOMENON
• Cruciate hemiparesis
• Suboccipital pain with radiation to neck and shoulders
• Bilateral papilledema due to raised ICT
2) Lesion at C5-C6
• Inverted supinator reflex
• Paraplegia
3) Lesion at C8-T1
• Wasting of small muscles of hand
• Horner’s syndrome
• Spastic paralysis of trunk and lower limbs
4) Lesion in the mid thoracic region
• Wasting of intercoastal muscles
• Spastic paralysis of abdominal muscles and lower limbs
5) Paraplegia – lesion below T10 vs Above T10
• On flexion of neck and contraction of abdominal muscles, if the umbilicus moves
2-3 cm upwards; indicates a T10 pathology
• Upper abd reflex preserved
• Lower abd reflex lost BEEVOR’s SIGN +
• Loss of tone of lower abd muscles
6) Lesion at T12-L1
• Cremasteric reflex lost
7) Lesion at L3-L4
• Wasting of quadriceps and hip adductors
• Knee jerk lost, ankle jerk present
• Extensor plantar, foot drop
8) Lesion at S1-S2
• Wasting of intrinsic muscles of foot
• Knee jerk preserved, ankle jerk is lost
• Plantar reflex is lost
9) Lesion at S3-S4
• Anal and bulbocavernous reflexes are lost
• Saddle anesthesia
Determination of the level of the lesion
• Below the level of lesion
UMN weakness, hyperreflexia, complete sensory loss
• At the level of lesion
LMN weakness, areflexia, root pain/ dysesthesia/ paresthesia
• Above the level of lesion
Complete sparing
Investigation
X-ray
CT scan
MRI
Myelogram
Biopsy
Bone scan
Blood and spinal fluid studies
CSF analysis
Routine cell count, glucose,protein,serological tests-syphilis
Froin’s syndrome-in spinalcanal blockage
(xanthochromia and Increase in protein as a result of which fluid –
coagulate spontaneously)
slight or no increase in cells , oligoclonal bands in multiple sclerosis
IgG index, CSF culture and sensitivity ,PCR for VZV,HSV-1,HSV-2 ,EBV,
CMV ,HHV-6,HIV
Immune mediated disorders
ESR,ANA,RA factor,antiphospholipid antibodies ,p-ANCA
Schirmer test, salivary gland scintigraphy ,lacrimal gland biopsy –
sjogrens syndrome
Demyeilinating disease
MRI brain , CSF oligoclonal bands,neuromyelitis optica antibody (anti-
aquaporin-4)
• MRI –investigation of choice for cord compression
-can differentiates syringomyelia from intramedullary tumors,
transverse myelitis etc
• CT-SCAN – detecting bony abnormalities like
osteomyelitis,metastasis,myeloma,osteosclerosis
• Chest-xray- lung carcinoma to rule out possible mets, mediastinal widening in
lymphoma
• Cerebral angiography-vascular abnormality
• Fundus – papilledema in intracranial tumor. Temporal pallor in multiple
sclerosis,
Therapeutic interventions
• Stabilisation /immobilisation
• Traction
-Gardner- well tongs
-Halo
Casts
Splints
Collars
Braces
Management of spinal cord injuries
A-B-C-D-E sequance
Airway management
-Use bag-valve-mask devise initially for airway compromise
Breathing
 Lesions above C5 level will cause partial to complete diaphragmatic
paralysis
 Any lesion above T12 may cause some airway compromise,
 Lesions at C5 and below will allow full diaphragmatic movement, but
intercostal muscles (T1) and abdominal muscles (T12) are affected
Circulation
Cardiac output is affected by external or internal hemorrhage.
To determine external bleeding , turn the patient in log-roll fashion
and quickly note the site of injury
Two signs of internal bleeding from abdominal trauma are abdominal
pain and muscular rigidity.
However, these signs may be masked in a patient with sensory and
motor deficits.
Exposure
• Patients with spinal cord injury become poikilothermic
• Because they lose the ability to regulate core body temperature
through vasodilatation and vasoconstriction
Neurological/orthopedic management
• Reduction
• Fixation
• Fusion
Fixation involves stabilizing vertebral fractures with wires ,plates and
other types of hardware
Rehabilitation and Long- Term issues
• Mobility
• Self care
• Exercise
• Spasticity
• Contractures
-Bed mobility
-Pressure relief
-Wheel chair transfer
References
• Guyton and hall textbook of medical physiology
• Localisation of clinical neurology ; Paul w Brazis
• Adams and victors Principles of neurology
• Harrison’s neurology in clinical medicine
Spinal cord disorders.pptx

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Spinal cord disorders.pptx

  • 1. SUBJECT SEMINAR APPROACH TO SPINAL CORD LESIONS GUIDE- Dr KALINGA B Sir STUDENT- Dr SATISH PATIL
  • 2. DEFINITION Insult to spinal cord resulting in change in the normal motor,sensory or autonomic function. This change either temporary or permanent.
  • 3. ANATOMY Spinal cord lies within protective covering of vertebral column. Begins just below foramen magnum of skull Ends opposite 2nd lumbar vertebra Below L2 continue as leash of nerve roots known as cauda equina. Prolongation of Pia matter forms Filum terminale
  • 4.
  • 5.
  • 6. Relation of spinal nerve roots to vertebrae Spinal cord level Corresponding vertebral body Upper cervical Same as cord level Lower cervical One level higher Upper thoracic Two levels higher Lower thoracic 2 – 3 levels higher Lumbar T10 – T12 Sacral T12 – L1
  • 7.
  • 8. Markers for sensory level T4 Nipple T10 Umbilicus T12 Pubic symphysis
  • 9.
  • 10. Conus medullaris • Conical structure • Continuous with filum terminale
  • 11. Cauda equina • Sheath of nerve root from lumbar and caudal segments in subarachnoid space enlargement. • Horse tail appearance
  • 12. Filum terminale • 20 cm long • Below the level of conus medullaris only piamater is continued as a fibrous cord.
  • 13. Reflex arc  Involuntary response to a stimulus.  Where sensory and motor nerves arise from cord Sensory fibers enter posterior Synapse in the grey matter Motor fibers leave anterior
  • 14.
  • 15. Spinal cord – blood supply • Anterior spinal artery Supplies ventral 2/3 of SC (anterior and lateral column) One in number • Posterior spinal artery Supplies dorsal 1/3 of SC (posterior column) Two in number
  • 16.
  • 17. Radicular arteries Upper half of cervical cord- no Lower cervical & first two thoracic- 4 Mid thoracic- 1 Lower thoracic to coccygeal- arterial radicularis magna
  • 18.
  • 19. Myelopathy – approach Symptoms • Limb weakness • Loss of pain and temperature • Loss of joint, position and vibration • Sharp shooting back pain (aggravated by cough) • Bowel and bladder incontinence
  • 20. Approach to patient History Onset 1.Sudden – trauma – Fracture dislocation of vertebrae infection – Epidural abscess vascular- Thrombosis of ASA , hematomyelia , Transverse myelitis , multiple sclerosis 2.Gradual – Neoplastic – meningioma , ependymoma , glioma, astrocytoma
  • 21. Sensory: 1.sacral sparing - intramedullary lesion) 2.radicular(root) pain- extramedullary lesion 3.poorly localised burning pain- intramedullary lesion Motor –limb involvement symmetrical or sequential -weakness more in proximal muscles ( difficulty in getting from sitting posture , climbing stairs , buckling of knees) - weakness is progressive or static H/O diurnal variation of weakness or fatiguability suggests – NMD(myesthenia gravis) H/O presence of stiffness or scissoring of limbs while walking, involuntary movements ( flexor spasms –UMN lesion)
  • 22. Sphincter disturbances - urgency,hesitancy – UMN type of bladder - Painful retention with overflow incontinence – LMN etiology - Early bladder involvement – intramedullary lesion
  • 23. Associated symptoms  Fever – infective causes  Seizures, delayed milestones  Associated specific symptoms – vit B12 deficiency History about  Preceding illness  Trauma  Prior vaccination
  • 24. Examination General physical examination o Lymph node ( TB, lymphoma, malignancy) o Temperature ( TB, acute transverse myelitis) o Skin ( café au lait spots in neurofibroma, trophic changes) Higher mental function o Affected in cerebral and degenerative diseases o Staccato speech in multiple sclerosis o Dysarthria in ALS and syringomyelia
  • 25. Cranial nerve examination • Affected in brain stem lesions • Optic atrophy – friedrich ataxia , multiple sclerosis • Nystagmus in multiple sclerosis • Pupillary changes in neurosyphilis • Difficulty on swallowing – ALS Tone and DTR • Increased in UMN • Decreased in LMN Sensory examination Proper examination of skull and spine
  • 26. Paraplegia • Pyramidal (UMN ) lesion – spastic paraplegia • Lower motor neuron ( LMN ) lesion – flaccid paraplegia
  • 27. Spastic paraplegia • Weakness of muscle along with increased tone • Occurs due to UMN disease Increased tone Exagerated DTR Plantar extension Further devided; -Paraplegia in extension -Paraplegia in flexion
  • 28. Paraplegia in extension Paraplegia in flexion Cause Pyramidal lesion Pyramidal or extrapyramidal Hypertonia More in extensors More in flexors Position of LL Extended Flexed Deep reflexes Exaggerated Less exagerated Clonus Present Absent Mass reflex Absent May be present Bladder precipitancy Autonomic bladder
  • 29. Causes Cortical Superior saggital sinus thrombosis Thrombosis of unpaired anterior cerebral artery Parasaggital meningioma Multiple sclerosis Space occupying lesion over motor area ; gliomas
  • 30. Myelopathy – classification Myelopathy Compressive Non compressive Extradural Intradural Extramedullary Intramedullary
  • 32. 1.Extradural Craniovertebral anomalies Cervical spondylosis Trauma Epidural abscess Aortic aneurysm compressing vertebral column Myeloma metastasis
  • 33. 2.Intradural Extramedullary lesion Intramedullary lesion Manifestations Stage 1: Root pain Stage 2: brown Sequard syndrome Stage 3: complete transection Motor UMN- early involvement with sacral sparing LMN- not involved UMN- late involvement LMN- due to AHC affection Sensory Dissociative sensory loss (spinothalamic lost, posterior column spared) ANS Not very common Early bowel and bladder involvement Trophic changes Not very common Common due to loss of pain Spinal deformity Spinal tenderness Present Absent CSF proteins Present Absent Examples Trauma Tumour/mets Aneurysm TB/ syphilis Neurofibroma Meningioma Arachnoid cyst Pachymeningitis
  • 34. Tumors • Most spinal tumors are extradural – about 85% Primary- spine Secondary – lung, breast,prostate,kidney ,thyroid Symptoms -pain -numbness -muscle weakness ,spasticity -loss of bowel and bladder control
  • 35. 1.Extradural tumors  Most common spinal tumor -85%  Mostly metastatic  Arise from osseous element of spinal column.  Primary: lung,breast, prostate and kidney.  Collapse of vertebrae distortion and narrowing. Ex ; 1. -Lymphoma 2. -Hemangioma 3. -Neuroblastoma
  • 36. 2.Intradural extramedullary tumors • Inside the dura but outside the spinal cord. • Arise from dural sheath around the cord or shwann cell sheath around the spinal root • Can grow into retroperitoneal or retropleural through intervertebral foramen Ex; Meningeoma Neurinoma
  • 37. 3.Intradural intramedullary tumors • Inside the spinal cord • Arise from glial elements of spinal cord • More common in children Ex Astrocytoma –most common intramedullary tumor of childhood. Ependymoma – most common intramedullary tumor of adulthood
  • 38. Non compressive myelopthies 1. Infections: TB/ HIV/ Lyme’s disease 2. Demyelinating disorders: Multiple sclerosis, ATM 3. Nutritional: SACD 4. Vascular: Anterior spinal artery syndrome, Leriche’s syndrome 5. Autoimmune: Lupus 6. Traumatic: Electric shock 7. Hereditary: Freidrich’s ataxia 8. Toxic: Lathyrism, flourosis
  • 39. Pott’s disease Infection reaches – Hematogenous spread - Adjescent paravertebral lymph nodes Involves two or more vertebral bodies Most common – lower thoracic and upper lumbar vertebra Collapsed vertebra or abscess cause compression of spinal cord leading to paraparesis X-ray shows decreased vertebral height collapsed vertebrae and irregular vertebral margins
  • 40.
  • 41. Acute transverse myelitis Gullian barre syndrome Lower limb > upper limb Progressive lower limb Proximal>distal Weakness Symmetrical Ascends to upper limbs and to face Sensory Sensory ataxia Normal Reflexes Hyperreflexia below the lesion Areflexia Bladder symptoms + - Band like sensation (Definite sensory level) -
  • 42. Friedreich’s ataxia and Sub acute combined degeneration FRIEDREICH’S ATAXIA SACD DRG -> Spinal cord -> Peripheral nerves Post column -> CST -> Peripheral neuropathy Reflexes Areflexia in lower limb Lost due to peripheral neuropathy Sensory Sensory ataxia Loss of vibration sense Tingling and numbness Weakness UMN type UMN type Associated findings Cardiomyopathy Optic atrophy Vitamin B12 deficiency Bilateral optic neuropathy Dementia
  • 43. Quadripares /quadriplegia Compressive 1.Trauma 2.Tumors - Metastatic - Primary 3.Vertebral disease -Disc Prolapse -Spondylosis -Pagets Disease -Deformity
  • 44. Non compressive • Infection – bacterial osteomyelitis, spinal abscess, HIV infection • Inflammatory – transverse myelitis, multiple sclerosis, SLE. • Vascular – Anterior spinal artery occlusion -Angioma -Av malformation • Others -Degenerative MND -Vit B12 deficiency
  • 45. Spinal cord injury 1.Primary - initial mechanism of injury 2. Secondary Ongoing progressive damage - Ischemia - Hypoxia - Microhemorrhage - Edema
  • 46. Statistics National Spinal Cord Injury Database ( NSCISC)  MVA - 38.2%% Falls - 32.3% Violence - 14.3% Sports - 7.8% Medical and surgical- 4.1% -55% cases occur in 16- 30 years of age - Among 81.6% are male.
  • 47. Mechanism of injury  Flexion  Hyperflexion  Compression  Rotation
  • 48. Flexion (hyper flexion) • Most common because of natural protection position
  • 49.
  • 50. Compression • Cause by force from above , as hit on head • Below as landing on butt • Usually affects lumbar region
  • 51. Rotation • Most unstable • Results in tearing of ligamentous structures that normally stabilize the spine • Usually results in serious neurologic deficits.
  • 52. Classification of spinal cord injury (Degree of injury ) 1. Complete 2. Incomplete  Central cord syndrome  Anterior cord syndrome  Brown sequard syndrome  Posterior cord syndrome  Cauda equina and conus medullaris
  • 53. Complete Features - Loss of voluntary movement of parts innervated by segment this is irreversible. - Spinal shock Deficits  Motor – spastic paralysis below level of injury  Sensory – loss of all sensation perception  Autonomic – vasomotor failure and spastic bladder
  • 54. Incomplete  Some function is present below site of injury  More favourable prognosis overall  Are recognizable pattern of injury, although they are rarely pure and variations occur
  • 55. Central cord syndrome  Injury to center of the cord by edema and hemorrhage  Motor weakness and sensory loss in all extremities  Upper extremities affected more
  • 56. Anterior cord syndrome  Injury to anterior cord  Loss of voluntary motor, pain and temperature perception below injury  Retains posterior column function (sensation of touch , position, vibration, motion)
  • 57. Posterior cord syndrome  Least frequent syndrome  Injury to the posterior(dorsal) column  Loss of proprioception, pain , temperature sensation.  Motor function below the level of lesion remain intact  Usually good power and sensation
  • 58. Brown – Sequard syndrome:  Hemisection of cord  Ipsilateral paralysis  Ipsilateral superficial sensation, vibration and proprioception loss.  Contralateral loss of pain and temperature perception.
  • 59.
  • 60. Cauda equina and conus medullaris Conus medullaris - injury to the sacral cord (conus) and lumbar nerve roots Cauda equina - injury to the lumbosacral nerve roots RESULT - areflexic ( flaccid) bladder and bowel , flaccid lower limbs
  • 61. Conus medullaris and cauda equina syndrome Conus medullaris syndrome Cauda equina syndrome Vertebral level L1-L2 L2-sacram Spinal level Sacral cord segment and roots Lumbosacral nerve roots Presentation Sudden and bilateral Gradual and unilateral Radicular pain Less severe More severe Low back pain More Less Motor strength Symmetrical,less marked hyperreflexic distal paresis of lower limb, fasciculation Symmetric , more marked ,areflexic paraplegia, atrophy more common Reflexes Ankle jerks affected Both knee and anke jerks affected Sensory Localised numbness to perianal area,symmetrical and bilateral Localised numbness at saddle area, asymmetrical,unilateral Sphincter dysfunction Early urinary and fecal incontinence Tend to present late
  • 62. Syringomyelia Cavitatory expansion of central canal of spinal cord (lower cervical) Associated with ARNOLD CHIARI MALFORMATION TYPE 1 (75%) Syringomyelia reaching medulla is syringobulbia
  • 63. Clinical features • Like an intramedullary lesion • HALF CAPE distribution of sensory loss Sensory loss along chest, upper arm, shoulder • ONION PEEL PATTERN ON FACE Loss of sensation on face • Compression of AHC Wasting of thenar eminence, forearm, arm • Spastic weakness • Horner’s syndrome (C8-T1)
  • 64.
  • 65. Chiari malformation Type 1 Herniation of cerebellear tonsils Associated with syringomyelia Type 2 (Arnold Chiari) Herniation of cerebellar vermis Usually accompanies by a lumbar myelomeningocele Type 3 Occipital encephalocele Usually with syringomyelia,tethered cord and hydrocephalous Type 4 Lack of cerebellar development Not compatible with life
  • 66.
  • 67. Clinical manifestations based on the level of the lesion 1) Lesion at foramen magnum • Around the clock weakness or ELSBERG PHENOMENON • Cruciate hemiparesis • Suboccipital pain with radiation to neck and shoulders • Bilateral papilledema due to raised ICT
  • 68. 2) Lesion at C5-C6 • Inverted supinator reflex • Paraplegia 3) Lesion at C8-T1 • Wasting of small muscles of hand • Horner’s syndrome • Spastic paralysis of trunk and lower limbs
  • 69. 4) Lesion in the mid thoracic region • Wasting of intercoastal muscles • Spastic paralysis of abdominal muscles and lower limbs 5) Paraplegia – lesion below T10 vs Above T10 • On flexion of neck and contraction of abdominal muscles, if the umbilicus moves 2-3 cm upwards; indicates a T10 pathology • Upper abd reflex preserved • Lower abd reflex lost BEEVOR’s SIGN + • Loss of tone of lower abd muscles
  • 70. 6) Lesion at T12-L1 • Cremasteric reflex lost 7) Lesion at L3-L4 • Wasting of quadriceps and hip adductors • Knee jerk lost, ankle jerk present • Extensor plantar, foot drop
  • 71. 8) Lesion at S1-S2 • Wasting of intrinsic muscles of foot • Knee jerk preserved, ankle jerk is lost • Plantar reflex is lost 9) Lesion at S3-S4 • Anal and bulbocavernous reflexes are lost • Saddle anesthesia
  • 72. Determination of the level of the lesion • Below the level of lesion UMN weakness, hyperreflexia, complete sensory loss • At the level of lesion LMN weakness, areflexia, root pain/ dysesthesia/ paresthesia • Above the level of lesion Complete sparing
  • 74. CSF analysis Routine cell count, glucose,protein,serological tests-syphilis Froin’s syndrome-in spinalcanal blockage (xanthochromia and Increase in protein as a result of which fluid – coagulate spontaneously) slight or no increase in cells , oligoclonal bands in multiple sclerosis IgG index, CSF culture and sensitivity ,PCR for VZV,HSV-1,HSV-2 ,EBV, CMV ,HHV-6,HIV
  • 75. Immune mediated disorders ESR,ANA,RA factor,antiphospholipid antibodies ,p-ANCA Schirmer test, salivary gland scintigraphy ,lacrimal gland biopsy – sjogrens syndrome Demyeilinating disease MRI brain , CSF oligoclonal bands,neuromyelitis optica antibody (anti- aquaporin-4)
  • 76. • MRI –investigation of choice for cord compression -can differentiates syringomyelia from intramedullary tumors, transverse myelitis etc • CT-SCAN – detecting bony abnormalities like osteomyelitis,metastasis,myeloma,osteosclerosis • Chest-xray- lung carcinoma to rule out possible mets, mediastinal widening in lymphoma • Cerebral angiography-vascular abnormality • Fundus – papilledema in intracranial tumor. Temporal pallor in multiple sclerosis,
  • 77. Therapeutic interventions • Stabilisation /immobilisation • Traction -Gardner- well tongs -Halo Casts Splints Collars Braces
  • 78. Management of spinal cord injuries A-B-C-D-E sequance Airway management -Use bag-valve-mask devise initially for airway compromise
  • 79. Breathing  Lesions above C5 level will cause partial to complete diaphragmatic paralysis  Any lesion above T12 may cause some airway compromise,  Lesions at C5 and below will allow full diaphragmatic movement, but intercostal muscles (T1) and abdominal muscles (T12) are affected
  • 80. Circulation Cardiac output is affected by external or internal hemorrhage. To determine external bleeding , turn the patient in log-roll fashion and quickly note the site of injury Two signs of internal bleeding from abdominal trauma are abdominal pain and muscular rigidity. However, these signs may be masked in a patient with sensory and motor deficits.
  • 81. Exposure • Patients with spinal cord injury become poikilothermic • Because they lose the ability to regulate core body temperature through vasodilatation and vasoconstriction
  • 82. Neurological/orthopedic management • Reduction • Fixation • Fusion Fixation involves stabilizing vertebral fractures with wires ,plates and other types of hardware
  • 83. Rehabilitation and Long- Term issues • Mobility • Self care • Exercise • Spasticity • Contractures -Bed mobility -Pressure relief -Wheel chair transfer
  • 84. References • Guyton and hall textbook of medical physiology • Localisation of clinical neurology ; Paul w Brazis • Adams and victors Principles of neurology • Harrison’s neurology in clinical medicine