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Spinal cord disorders Anatomical Approach

Anatomical approach to spinal cord disease

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Spinal cord disorders Anatomical Approach

  1. 1. SPINAL CORD DISORDERS ANATOMICAL APPROACH Dr PS Deb MD, DM Director Neurology Guwahati Neurological Research Institute Assam, India
  2. 2. SPINAL CORD  Information highway between brain and body  Extends through vertebral canal from foramen magnum to L1  Each pair of spinal nerves receives sensory information and issues motor signals to muscles and glands  Spinal cord is a component of the Central Nervous System while the spinal nerves are part of the Peripheral Nervous System
  3. 3. SPINAL CORD FUNCTIONS  Conduction  bundles of fibers passing information up and down spinal cord  Locomotion  repetitive, coordinated actions of several muscle groups  central pattern generators are pools of neurons providing control of flexors and extensors (walking)  Reflexes  involuntary, stereotyped responses to stimuli (remove hand from hot stove)  involves brain, spinal cord and peripheral nerves
  4. 4. SPINAL CORD - ANATOMY  Runs through the vertebral canal  Extends from foramen magnum to second lumbar vertebra  Regions  Cervical  Thoracic  Lumbar  Sacral  Coccygeal  Gives rise to 31 pairs of spinal nerves  All are mixed nerves  Not uniform in diameter  Cervical enlargement: supplies upper limbs  Lumbar enlargement: supplies lower limbs  Conus medullaris- tapered inferior end  Ends between L1 and L2  Cauda equina - origin of spinal nerves extending inferiorly from conus medullaris
  5. 5. SPINAL CORD GROSS ANATOMY Spinal cord Special Segments Cervical enlargement C5-T1 Lumber enlargement L3-S2 Conus S3-Co Epiconus L4-S2 Cauda equina L3-Cx
  6. 6. SPINAL CORD: LONGITUDINAL EXTENT  Spinal cord stretches from foramen magnum till coccyx in fetal life then due to growth of spine it fall short  At 3rd fetal month up to coccyx  At birth lower border of L3  Adult spinal cord ends at lower border of L1 body
  7. 7. SPINAL CORD LEVEL /SPINAL LEVEL Spine Cord Upper cervical same level Lower cervical + 1 Upper thoracic + 2 Lower thoracic +3 T12 Lower lumber L1 Sacral cord
  8. 8. COVERING OF SPINAL CORD  Connective tissue membranes  Dura mater: outermost layer; continuous with epineurium of the spinal nerves  Arachnoid mater: thin and wispy  Pia mater: bound tightly to surface  Forms the filum terminale  anchors spinal cord to coccyx  Forms the denticulate ligaments that attach the spinal cord to the dura  Spaces  Epidural: external to the dura  Anesthestics injected here  Fat-fill  Subdural space: serous fluid  Subarachnoid: between pia and arachnoid  Filled with CSF
  9. 9. SPINAL CORD TRANSVERSE SECTION
  10. 10. SPINAL CORD TRANSVERSE SECTION  Anterior median fissure and posterior median sulcus  deep clefts partially separating left and right halves  Gray matter: neuron cell bodies, dendrites, axons  Divided into horns  Posterior (dorsal) horn  Anterior (ventral) horn  Lateral horn  White matter  Myelinated axons  Divided into three columns (funiculi)  Ventral  Dorsal  lateral  Each of these divided into sensory or motor tracts
  11. 11. SPINAL CORD TRANSVERSE SECTION  Commissures: connections between left and right halves  Gray with central canal in the center  White  Roots  Spinal nerves arise as rootlets then combine to form dorsal and ventral roots  Dorsal and ventral roots merge laterally and form the spinal nerve
  12. 12. SPINAL CORD GRAY MATTER  Dorsal half – sensory roots and ganglia  Ventral half – motor roots  Based on the type of neurons/cell bodies located in each horn, it is specialized further into 4 regions  Somatic sensory (SS) - axons of somatic sensory neurons  Visceral sensory (VS) - neurons of visceral sensory neur.  Visceral motor (VM) - cell bodies of visceral motor neurons  Somatic motor (SM) - cell bodies of somatic motor neurons
  13. 13. GRAY MATTER OF SPINAL CORD  Lamina I - posteromarginal nucleus  Lamina II - substantia gelatinosa of Rolando  Lamina III, IV - nucleus proprius  Lamina V, VI  Lamina VII - intermediate gray intermediolateral cell column (ILM) Clarke’s column (Nucleus dorsal intermediomedial cell column (IMM)  Lamina VIII  Lamina IX - anterior horn (motor) cell  Lamina X - gray commissure
  14. 14. SPINAL CORD SEGMENTS
  15. 15. WHITE MATTER OF SPINAL CORD  Divided into three funiculi (columns) – posterior, lateral, and anterior  Columns contain 3 different types of fibers (Ascend., Descend., Trans.)  Fibers run in three directions  Ascending fibers - compose the sensory tracts  Descending fibers - compose the motor tracts  Commissural (transverse) fibers - connect opposite sides of cord  Pathways decussate (most)  Most consist of a chain of two or three neurons  Most exhibit somatotopy (precise spatial relationships)  All pathways are paired  one on each side of the spinal cord
  16. 16. WHITE MATTER TRACTS
  17. 17. CORTICOSPINAL TRACT  Originate in the precentral gyrus of brain (aka, primary motr area)  I.e., cell body of the UMN located in precentral gyrus  UMN synapses in the anterior horn with LMN  Some UMN decussate in pyramids = Lateral corticospinal tracts  Others decussate at other levels of s.c. = Anterior corticospinal tracts  LMN (anterior horn motor neurons)  Exits spinal cord via anterior root  Activates skeletal muscles  Regulates fast and fine (skilled) movements
  18. 18. EXTRAPYRAMIDAL TRACTS  Includes all motor pathways not part of the pyramidal system  Upper motor neuron (UMN) originates in nuclei deep in cerebrum (not in cerebral cortex)  UMN does not pass through the pyramids!  LMN is an anterior horn motor neuron  This system includes  Reticulospinal tracts – originates at reticular formation of brain; maintain balance  Rubrospinal tracts – originate in ‘red nucleus’ of midbrain; control flexor muscles  Tectospinal tracts - originate in superior colliculi and mediate head and eye movements towards visual targets (flash of light)  Vestibulospinal Tract – muscle tone in relation to head and neck movement  Regulate:  Axial muscles that maintain balance and posture  Muscles controlling coarse movements of the proximal portions of limbs  Head, neck, and eye movement
  19. 19. Extrapyramidal tracts
  20. 20. ASCENDING PATHWAY  The central processes of first-order neurons branch diffusely as they enter the spinal cord and medulla  Some branches take part in spinal cord reflexes  Others synapse with second-order neurons in the cord and medullary nuclei  The nonspecific and specific ascending pathways send impulses to the sensory cortex  These pathways are responsible for discriminative touch (2 pt. discrimination) and conscious proprioception (body position sense).  The spinocerebellar tracts send impulses to the cerebellum and do not contribute to sensory perception
  21. 21. CRANIAL SOMESTHETIC SENSATION
  22. 22. DIRECT SPINOTHALAMIC TRACT  Include the lateral and anterior spinothalamic tracts  Lateral: transmits impulses concerned with pain and temp. to opposite side of brain  Anterior: transmits impulses concerned with crude touch and pressure to opposite side of brain  1st order neuron: sensory neuron  2nd order neuron: interneurons of dorsal horn; synapse with 3rd order neuron in thalamus  3rd order neuron: carry impulse from thalamus to postcentral gyrus
  23. 23. INDIRECT SPINOTHALAMIC TRACT
  24. 24. SPINOHTALAMIC PAIN TYPES  Fast Pain Slow Pain  Sharp, pricking Dull, burning  Group III (A) fiber Group IV (C) fiber  Short latency Slower onset  Well localized Diffuse  Short duration Long duration  Less emotional Emotional, autonomic response  Not blocked by morphine Blocked by morphine  Neospinothalamic Tract Paleospinothalamic Tract
  25. 25. 13-27 SPINORETICULAR TRACT  Pain signals from tissue injury  Decussate in spinal cord and ascend with spinothalamic fibers  End in reticular formation (medulla and pons)  3rd and 4th order neurons continue to thalamus and cerebral cortex
  26. 26. SPINOCEREBELLAR TRACTS Spinocerebellar Tract  Proprioceptive signals from limbs and trunk travel up to the cerebellum  Second order nerves ascend in ipsilateral lateral column.Transmit info. about trunk and lower limb muscles and tendons to cerebellum  No conscious sensation Anterior SCbllT (superior cerebellar peduncle) anterior spinocerebellar tract anterior white commissure posterior root Posterior SCbllT Inferior cerebellar peduncle cuneocerebellar tract (upper body) posterior white column posterior root
  27. 27. (A) THE DORSAL (POSTERIOR) SPINOCEREBELLAR TRACT. (B) THE CUNEOCEREBELLAR TRACT. SEE TEXT FOR DETAILS.
  28. 28. VENTRAL SPINOCEREBELLAR TRACT
  29. 29. POST. COLUMN Dorsal Column Tract 1. AKA Medial lemniscal pathway 2. Fibers run only in dorsal column 3. Transmit impulses from receptors in skin and joints 4. Detect discriminative touch and body position sense =proprioception 1st order neuron - a sensory neuron synapses with 2nd order neuron in nucleus gracilis and nucleus cuneatus of medulla 2nd order neuron.- an interneuron decussate and ascend to thalamus where it synapses with 3rd order neuron 3rd-order (thalamic neurons) transmits impulse to somato- sensory cortex (postcentral gyrus)
  30. 30. VASCULAR SUPPLIES OF SPINAL CORD Posterior spinal artery Anterior spinal artery Origin Vertebral arteries inside the skull Posterior inferior cerebellar artery Formed by the union of the 2 arteries which are arising from the vertebral artery inside the skull Position Descends on the posterior surface of the spinal cord close to the posterior nerve roots Descends on the anterior surface of the spinal cord within the anterior median fissure Supply Posterior 1/3 of the spinal cord Anterior 2/3 of the spinal cord Remark Small in the upper thoracic region Small in the upper and lower thoracic segment of the spinal cord Risk of ischemia T1-T3 segments if the segmental or radicular arteries are occluded T4 & L1 segments if the segmental or radicular arteries are occluded
  31. 31. SPINAL CORD DISORDER CLINICAL PRESENTATION
  32. 32. FEATURES SUGGESTIVE OF SPINAL CORD DISEASE System Features Motor – weakness Acute Flaccid Chronic Spastic Sensory - Loss Spinothalamic Below the level contralateral Post. Column Ipsilateral below the level Autonomic - Loss Acute Retention, flaccid Chronic Automatic, spastic Reflex - Altered Acute – Loss of all reflex Chronic Deep – exaggerated Superficial – Altered – abdominal, cremastic absent, plantar extensor Other features Level of consciousness - maintained Cognition - Normal Cranial nerve - Normal
  33. 33. SPINAL CORD SYNDROMES 1. Nature of pathology 1. Compressive 1. Intramedullary 2. Extra medullary 1. Intradural 2. Extradural 2. Non compressive 2. Anatomical location of lesion 1. Transverse 2. Longitudinal 3. Progression and onset of symptoms 1. Acute 2. Chronic 4. Age of onset 1. Childhood 2. Adulthood 3. Elderly
  34. 34. SPINAL CORD: EXTRINSIC  Radicular involvement  Asymetric, progression in inverted U pattern  Ipsi Lateral Hemiplegia,  contralateral spinothalamic lesion  Ipsilateral posterior column sensory loss
  35. 35. SPINAL CORD: INTRINSIC  Dissociated anesthesia  Jacket Anesthesia  Long tract sign  Sacral sparing  Ant. Horn cell involvement  Symmetrical/ Asymmetrical  Bladder involvement
  36. 36. signs intramedullary extramedullary Radicular pain unusual common Vertebral pain unusual common Funicular pain common Less common Umn Sign +, late +, early Lmn sign +++, diffuse Unusual, segmental Paraesthesia progr descending ascending sphincter early late Trophic common unusual
  37. 37. Extramedullary Intramedullary Motor a)UMN signs Common Late b)LMN signs 1or2segments at the site of root compression wide (Ant horn cell) Sensory a)Pain Root pain Funicular pain b)Dissociated sensory loss Absent present c)Sacral sensation Lost Preserved d)Joint sensation Lost Late involvement e)Lhermitte`s sign present absent Autonamic involvement – Bowel and Bladder Late Early Intradural Extradural Mode of onset Asymmetrical , acute,rapid malignant Symmetrical,slow, progressive benign Vertebral No Pain and gibbus Pain and Gibbus
  38. 38. COMPRESSIVE MYELOPATHIES  Extradural  Bone  Neoplastic  Secondries  Osteosarcoma  Infection  Tuberculosis  Pyogenic  Disc  Prolapse  Stenosis  Anomalies  Meningies  Inflammation  Arachnoiditis  Tubercular  Syphilitic  Toxic  Abscess  AIDS  Tumor  Dermoid  Epidermoid  Lipoma
  39. 39. COMPRESSIVE MYELOPATHY  Intradural  Meningioma  Neurofibroma  Intramedullary  Glioma  Ependymoma  AVM  Hemangioblastoma  Developmental Traction  Diastomatomyelia  Tethered Cord
  40. 40. MYELO-OPTIC NEURITIS  Demyelinating  Multiple sclerosis  Devic’s disease  Nutritional  Subacute combined degeneration  Pellagra  Tropical spastic paraplegia  Toxic  Lathyrism  SMON  Hereditary  Familial spastic paraplegia with optic atrophy
  41. 41. MYELORADICULITIS  Infection  Tubercular (Arachnoiditis, Pott’s spine)  Pyogenic  Syphilitic  Spine  CV junction anomaly  Narrow canal  Toxic
  42. 42. TRANSVERSE CORD SYNDROMES
  43. 43. A. TRANSACTION OF CORD  Etiology  Trauma  Demyelination  Vascular  Tumor  Infection  Radiation
  44. 44. CLINICAL FEATURES  At the level of lesion  Band like radicular pain or  Segmental paraesthesia  Lower motor signs  Localised vertebral spine pain- destructive lesions  Below the level of lesion  Sensory loss (all modalities)  Motor loss (Paraplegia, Quadriplegia)  Arflexia -> hypereflexia  Bladder bowel involvement
  45. 45. STAGES OF ACUTE CORD SYNDROME (RIDDOCH)  Stage of spinal shock  Motor autonaumic areflexia for 1-6weeks  Sometimes last longer or permanent with minimal recovery  Mechanism  Release of supraspinal control  Vascular  Stage of hightended activity  Below the lesion  Tendon hyperreflexia  Babinski sign  Flexor spasm  Reflex bladder bowl mass reflex  Increased by infection and nociceptive stimuli  Above the lesion  Autonaumic dysreflexia- Disinhibited sympathetic adrenal and medullary discharge-> sweating flussing hypertension, bradycardia
  46. 46. B. CENTRAL CORD SYNDROME  Etiologies 1. Trauma: Especially with 1. Cervical arthritis 2. Older patients 3. Spondylitic myelopathy 2. Syringomyelia 3. Neoplasm: 1. Metastatic, Glioma, lymphoma
  47. 47. CLINICAL FEATURES  Sensory loss  Pain & temperature (crossing fiber of spinothalamic tract) > Thermo anaesthesia, analgesia in a ”vest like” or “suspended” bilateral distribution with preservation soft touch sensation and proprioception-- - dissociation of sensory loss  Sparing: Sacral  Weakness: Arms > legs (Man in Barrel)  May occur in absence of spinal fracture
  48. 48. PROGRESSION OF CENTRAL CORD  Forward extension of disease anterior horn cells inv- segmental neurogenic atrophy, paresis, areflexia  Lateral extension I/L horner syndrome kypho scoliosis spastic paralysis  Dorsal extension I/L position sense, vibratory loss  Extreme venterolateral extension thermo anaesthesia, analgesia with sacral sparing  Neuropathic arthropathy  Pain
  49. 49. C. ANTERIOR CORD SYNDROME  Etiology:  Anterior spinal artery territory ischemia  Disc: osteophytes  Clinical Feature  Loss: Motor function Legs > Arm (Corticospinal tract)  Pain & temperature sensation loss with preservation: Position sense (Dissociated anesthesia)
  50. 50. D. ANTERIOR HORN CELL SYNDROME  Aterior horn cell, cranial motor nuclei involved  Autosomal recessive spinomuscular atrophy  Diffuse weakness and atrophy, fasciculations of trunk and extremities  Muscle tone& DTR ↓  Sensation intact
  51. 51. COMBINED ANTERIOR HORN CELL AND PYRAMIDAL TRACT DISEASE  Progressive diffuse LMN signs with UMN dysfunction  Striated muscles except pelvic floor mucles affected  U/L, muscles of hands and foot are involved  Sparing rectal and urethral sphincter  Bulbar and pseudobulbar inv super imposed
  52. 52. E. POSTERIOR CORD SYNDROME  Etiology  Posterior spinal artery damage  Diffuse atherosclerosis: Deficient collateral perfusion  B12 deficiency  Lipoma  Ligamentum flavum hypertrophy  Bimondo’s post column degeneration  Tabes dorsalis  Clinical Features  Loss: Position sense  Relative preservation: Motor, pain & temperature  Prognosis: Better than anterior syndrome
  53. 53. F. POSTERO LATERAL COLUMN DISEASE  Etiology  SACD- B12 def  Vacuolar myelopathy- AIDS-HTLV 1, tropical spastic paraparesis  Cervical spondylosis  Clinical  paraesthesia,  diffficulty with gait , balance,  loss of vibration and proprioception, sensory ataxia, rombergs +,  bladder atony,  reflexes lost or hypo active – super imposed peripheral neuropathy
  54. 54. G. ANTERIOR HORN CELL SYNDROME  Aterior horn cell, cranial motor nuclei involved  Autosomal recessive spinomuscular atrophy  Diffuse weakness and atrophy, fasciculations of trunk and extremities  Muscle tone& DTR ↓  Sensation intact
  55. 55. H. COMBINED ANTERIOR HORN CELL AND PYRAMIDAL TRACT DISEASE  Progressive diffuse LMN signs with UMN dysfunction  Striated muscles except pelvic floor mucles affected  U/L, muscles of hands and foot are involved  Sparing rectal and urethral sphincter  Bulbar and pseudobulbar inv super imposed
  56. 56. I. BROWN-SÉQUARD: HEMICORD INJURY  Etiologies  Tumor: Dumbbell Facet; Luschka joint  Trauma: Penetrating  Radiation  Decompression sickness  Clinical Features  Ipsilateral loss  Weakness  Position sense  Contralateral loss  Pain & temperature
  57. 57. LONGITUDINAL CORD SYNDROMES
  58. 58. FORAMEN MAGNUM SYNDROME & LESIONS OF UPPER CERVICAL CORD:  Sub occipital pain in C2 distribution, neck stiffness, electric shock like sensation sub occipital paraesthesia, syringo myelic type of sensory dissociation, finger tip numbness and tingling Spastic tetraparesis, long tract sensory findings, lower cranial nerve palsy “around the clock presentation of UMN type of weakness foramen magnum lesion- down beat nystagmus, papilloedema ,cerebelar ataxia causes: tumour,cx spondylosis, basilar invagination in pagets disease , syrinx, C1C2 subluxation, chiari, MS
  59. 59. Pyramidal tract decussates at cervicomedullary jn- lesion at this place causes HEMIPLEGIA CRUCIATA, onion skin pattern of facial sensory loss, respiratory insufficiency, bladder dysfunction Compressive lesion of C1-C5 cord segment may compromise the cranial nerve 11 C3-C5 lesion produces diaphragmatic paralysis High cervical cord lesion- respiratory arrest
  60. 60.  Lesions of C5-C6: LMN signs at corresponding segment level. UMN sign below the lesion, LMN paresis of arm associated with spastic para paresis of lower extremities. C5 level: Diaphragmatic function compromised BJ&BRJ –ve TJ & FFR ++++ Inversion of brachio radialis reflex Sensory loss entire body below neck and anterior shoulder C6 level: BJ,BRJ,TJ –ve & FFR ++++ Sensory loss samme as that of C5 lesion sparing the lateral part of arm
  61. 61.  Lesion at C7: Diaphragm fn normal Paresis of flexors and extensors of wrist and fingers BJ,BRJ-Normal, FFR++++ Paradoxical triceps jerk Sensory loss at /below 3rd 4th finger  Lesion at C8 T1: Weakness of small muscles of hands with spastic paraparesis C8 inv- TJ &FFR-ve T1 inv-TJ –Normal, FFR-ve U/L or B/l horner syndrome Sensory loss starts from fifth digit
  62. 62.  Lesion of thoracic segment level: Root pain , paraesthesia mimicking intercostal neuralgia Segmental LMN paralysis Paraplegia and sensory loss below a thoracic level Bladder, bowel sexual dysfunction Lesion above T5- orthostatic hypotension, episodic autonomic dysreflexia Lesion at T10- +ve Beevors sign Lesion at T6- abdominal reflex –ve Lesion at T10 – upper, middle part +ve Lesion at T12- abdominal reflex intact
  63. 63.  Lesion at L1: All muscles of lower extremities – weak Lower abd musc- Internal oblique, tr abd weak Sensory loss – both lower limbs up to groin, to a level above buttocks Chronic lesion- patellar++++, ankle++++  Lesion at L2: Spastic paraparesis Cremasteric reflex↓↓, patellar reflex ↓↓ Ankle jerk ++++ Sensation in upper anterior aspect preserved
  64. 64.  Lesion at L3: Some preservation of hip flexion, adduction KJ ↓↓, ankle++++ Sensation upper anterior aspect of thigh normal  Lesion at L4: Better hip flexion, adduction Able to stand stabilising knee KJ↓↓ , ankle++++ Sensation normal in anterior aspect of thigh, superomedial aspect of knee  Lesion at L5: Normal hip flexion, adduction KJ- normal, ankle++++ pt extends knee against resistance Sensation normal in antr aspect of thigh, medial aspect of legs ankle and sole
  65. 65.  Lesion at S1: Weakness of triceps surae, flexors of foot, and small muscles of foot Ankle reflex↓↓, KJ-normal Sensory loss- sole, heel, outer aspect of foot and ankle, medial aspect of calf, posterior thigh, outer aspect of saddle area also anaesthetic  S2 lesion: Triceps surae spared, flexors of toes, small muscles of foot weakness Ankle jerk ↓↓ Sensory loss- upper part of dorsal aspect of calf, dorsolateral aspect of thigh and saddle area
  66. 66. ROOT SYNDROMES Root Sensation Index Muscle Reflex Comments C3/4 Pain or hypalgesia in shoulders Paresis of diaphragm, occasionally rhomboids None C3 anterior diaphragm, C4 posterior diaphragm C5 Pain or hypalgesia laterally over upper arm and shoulders Paresis of deltoid, supraspin-atus, infra- spinatus, rhomboids Diminished biceps reflex Common causes include brachial neuritis, upper plexus injury, cervical spondylosis C6 Pain or hypalgesia of radial forearm, thumb, and index finger Paresis of biceps, brachialis, brachiorad-ialis, Extensor carpi radialis Diminished biceps, brachiorad ialis reflex Common causes include spondylosis, acute disc lesion (20%) C7 Pain or hypalgesia over triceps, mid- forearm and middle finger Paresis of triceps, latissimus dorsi, pectoralis major, ext. carpi ulnaris , flex. carpi radialis Diminished or absent triceps reflex Common causes includes acute disc lesions (70%), spondylosis, DDX includes CTS (triceps reflex present) C8 Pain or hypalgesia over ulnar forearm, 4th/5th digits Paresis of flex. dig. sup. & profundus, flex. poll. longus, flex. carpi ulnaris Diminished finger jerk (Hoffmans or Tromner) Caused rarely by spondylosis or acute disc lesion; DDX includes ulnar nerve palsy
  67. 67. ROOT SYNDROMES Root Sensation Index Muscle Reflex Comments T1 Pain or hypalgesia from axilla to olecranon Paresis of all small hand muscles and hypothenar wasting None Common causes include outlet syndrome, pancoast tumor, metastatic Ca of deep cervical nodes L3 Pain or hypalgesia across upper anterior thigh Paresis of quadriceps femoris Patellar reflex decreased or absent DDX includes femoral nerve palsy L4 Pain or hypalgesia from lateral thigh, over patella to medial calf and inner foot Paresis of quadriceps femoris, and tibialis anterior Patellar reflex diminished 5% lumbar discs, DDX includes femoral nerve palsy L5 Pain or hypalgesia from postero- lateral thigh to lateral calf to dorsum of foot Paresis of EHL, occ EDB Posterior tibial reflex decreased; useful only if elicitable on other side 40% lumbar discs; DDX includes peroneal nerve palsy S1 Pain or hypalgesia from posterior thigh down to lateral aspect and sole of foot Paresis of triceps surae, hamstrings, gluteus maximus Achilles tendon reflex decreased 45% lumbar discs
  68. 68. I. CONUS MEDULLARIS: INFERIOR CORD Etiology 1. Tumor 2. Compression 3. Ischemia Clinical features 1. Onset: Rapid 2. Symmetric defects 3. Pain: Inconstant; Perineum & thighs 4. Weakness: Sacral 5. Sensory 6. Saddle (sacral distribution)May be dissociated 7. Tendon reflex loss: Ankle > Knee 8. Bladder involvement; Impotence: Consistent; Early
  69. 69. J. CAUDA EQUINA Etiology 1. Compression: Tumor 2. Arachnoiditis Clinical features 1. Onset: Progressive; Slow; Unilateral 2. Asymmetric 3. Pain: Severe; Radicular distribution 4. Sensory loss 1. All modalities 2. Lumbar > sacral 5. Weakness: Lumbar > sacral 6. Fasciculations: Common 7. Tendon reflex loss: Knee > Ankle 8. Bladder involvement: Occasional; Late 9. Spinal injury: Below L2  Rule out: Lumbosacral plexus lesion
  70. 70. CONUS /CAUDA LESIONS Conus lesion Cauda lesion Spont pain -ve, B/L +ve, severe, Radicular, U/L sensory Saddle, B/L saddle., U/L deficit dissociation All forms affected Motor loss Symmetric, Asymmetric , atro fasciculations Phy, no fasciculn DTR Ankle -ve KJ, ankle -ve Bowel,bld early late trophic +ve -ve Sex fn impaired Less impaired onset Sudden. b/l Gradual, u/l
  71. 71. ANTERIOR SPINAL ARTERY SYNDROME:  Territory – anterior funiculi, anterior horn, base of the dorsal horn, peri ependymal area, antero medial aspect of lateral funiculi  Lower thoracic sement and conus- vulnerable  Abrupt onset of radicular pain, girdle pain  Flaccid quadriplegia, paraplegia  Bowel bladder dysfunction  Thermo anaesthesia analgesia  Position vibration light touch preserved  Painful burning dysasthesia  Watershed boundary zoneT1-T4, L1, central white matter of anterior funiculi
  72. 72. POSTERIOR SPINAL ARTERY SYNDROME:  Uncommon  Loss of position , proprioception, vibration  Loss of segmental reflexes  Pain , temperature – preserved  Motor function- preserved  Rarely – U/L posterior horn, lateral spinal cord inv  Lacunar infarct:  Isolated focal motor/sensory deficits in extremities  Hypoxic myelopathy:  Slowly progressive paraparesis/quadriparesis  Hemoynaemic TIA:  spinal cord claudication
  73. 73. VENOUS SPINAL CORD INFARCTION:  Impaired venous drainage, insitu thrombosis  Retrograde emboli  Chronic venous hypertension- irreversible spinal injury  Slowly progressive myelopathy, varying degrees of pain and sensory disturbances in the extremities, bladder bowel disturbances
  74. 74. THANKS

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