Dr. M. Sofi MD;FRCP(London); FRCPEdin; FRCSEdin

 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 Overview of Spinal Cord

The spinal cord has two major functions:  Carrying information: Spinal cord transmit information from body organs and external stimuli to the brain and send information from the brain to other areas of the body Coordinating reflexes: coordinates reflexes without the involvement of the brain, thus, the spinal cord has both communicative and integrative functions.  Reflex actions are automatic, unlearned, involuntary, and inborn responses.  These actions are sudden in nature and have a purpose of protecting the individual or his organs from sudden danger Functions of the Spinal Cord

Somato-sensory Organization

Lateral Coticospinal Tract Anterior Corticospinal Tract Rubrospinal Reticulaospinal Olivospinal Vestibulospinal Extrapyramidal Tracts Descending TractsPyramidal tracts Somatosensory organization

Somato-sensory Organization Ascending tracts Sensory & Ascending Pathways Dorsal Column Medial Lemniscus  Gracile fasciculus  Cuneate fasciculus Spinocerebellar Tracts  Posteriors pinocerebellar  Anterior spinocerebellar Anterolateral System  Lateral spinothalmic tract  Anterior spinothalmic tract  Spino-olivary tract

BLOOD SUPPLY SPINAL CORD

Spinal shock is a loss of sensation accompanied by motor paralysis with initial loss but gradual recovery of reflexes, following a spinal cord injury (SCI) – most often a complete transaction.  Reflexes in the spinal cord caudal to the SCI are depressed hyporeflexia/areflexia), while those rostral to the SCI remain unaffected.  ‘Shock' in spinal shock does not refer to circulatory collapse, and should not be confused with neurogenic shock. Paraplegia & Spinal cord syndromes PhaseTimePhysical exam findingUnderlying physiological event 10-1dAreflexia/HyporeflexiaLoss of descending facilitation 21-3dInitial reflex returnDenervation supersensitivity 31-4wHyperreflexia (initial)Axon-supported synapse growth 41-12mHyperreflexia, SpasticitySoma-supported synapse growth

Paraplegia & Spinal cord syndromes Classification of etiology LMN type/Flaccid paraplegia UMN type/ Spastic paraplegia Cortical lesion Spinal cord lesion Non-compressive Myelopathy Compressive Myelopathy Tumor Falx Cerebri Superior Sagital Sinus Thrombosis

Paraplegia & Spinal cord syndromes Classification of etiology COMPRESSIVE MYELOPATHY EXTRAMEDULLARYINTRAMEDULLARY EXTRADURAL INTRADURAL Syringomyelia, Ependymymoa, Glioma, Astrocytoma DISCVERTEBRAL Meningoma, Neurofibroma, Arachnoditis

Paraplegia & Spinal cord syndromes Classification of etiology Non-compressive myelopathies INFAMMATORY NONINLAMMATORY INFECTIOUS: VIRAL, BACTERIAL,FUNGAL PARASTIC AUTOIMMUNE: SLE, SJOGREN, SARCOIDOSIS, BECHET S, MCTD DEMYELINATING: MS,NMO, ADEM, POST VIRAL POST VACCINIAL PARANEOPLASTIC INHERITED: HSP, INHERITED METABOLIC DISORDERS METABOLIC: VIT B12,COPPER,FOLATE,AIDS ASSOCIATED, VIT E DEFICIENCY TOXIC: CASSAVA, LATHYRISM,FLUOROSIS, SMON, NITROUS OXIDE VASCULAR: ANT SPINAL ARTERY THROMBOSIS, AVM, DURAL AV FISTULA

Paraplegia & Spinal cord syndromes Differences between extradural and intradural lesions Extradural Mnemonic – (3 Ps)  Pain present - (root pain & spinal tenderness)  Pyramidal involvement – early  Protein in CSF high Intradural  Dissociated anesthesia  Bladder involvement early  Not so high protein  Symmetrical involvement  Trophic ulcers common Determining level of lesion in cord compression  Sensory level  Motor level  Reflex level  Root pain – dermatome  Type of bladder involvement Sensory level – below that level, sensory impairment of loss Motor level – Beevor’s sign indicates T10 lesion Reflex level – Inverted supinator C5 lesion

Vascular disorders of spinal cord  Ischemic disorders of spinal cord  Primary ischemia: atherosclerosis/vasculitis  Secondary ischemia: SOL, disorders of aorta  Decompression sickness  Spinal hemorrhage: SAH, SDH, EDH, hematomyelia  Spinal AVM/Dural AV fistula Inflammatory disorders spinal cord  Acute TM: viral, bacterial, fungal, post-infectious  Myelitis of chronic disorders: MS  Myelitis of systemic disorders: Behcet’s  Medulary compression:  Epidural abscess  Subdural abscess  Spondilodiscitis Paraplegia & Spinal cord syndromes

Non-inflamatory spinal space occupying lesions  Disc prolapse  Neoplasms Non-spinal disorders  Acute poliradiculitis Guillain Barre  Hyper/Hypokalemic paralysis  Parasigital cortical syndromes:  Bilateral infarctions Toxic or allergic disorders of spinal cord  Subacute-myelo-optico- neuropahty (SMON) caused by clioquinol  Late myelopathy after chemonucleolysis Elsberg phenomena: In cervical myelopathy there is first weakness ipsilateral arm, then ipsilateral leg then contralateral leg and lastly contralateral arm. Paraplegia & Spinal cord syndromes

Clinical approach to Spinal cord syndromes What is the onset of paraplegia Is it acute within minutes or hours? Sub-acute within days or weeks? Is it chronic within months or years? Was there a history of trauma? Fall from a Height? Road traffic accident? Direct injury to spine?

Clinical approach to Spinal cord syndromes Symmetry of symptoms? Is motor weakness symmetrical? Is sensory symptoms symmetrical? Or they are asymmetrical? Any wasting or fasciculations? Anywhere in the body? Small muscles of the hand? Thigh and gluteal muscles?

Clinical approach to Spinal cord syndromes Is there a history of root pains? Is it unilateral or bilateral? Does it radiate to Limbs? Does it aggravate with coughing? Any pyramidal tract involvement? Buckling of knees while walking? Slipping of foot Wear? Tipping on small Objects?

Clinical approach to Spinal cord syndromes History of vaccinations? Anti Rabies Vaccination? Polio vaccination?Others? History of increased ICT Fever and headache? Projectile vomiting? Seizures or loss of consciousness?

Clinical approach to Spinal cord syndromes What is the nature of neurological deficit? Is it a? Paraplegia? Tetraplegia? Brain stem lesion? Consider and exclude Guillian Barre Syndrome Cerebral diplgia?

Clinical approach to Spinal cord syndromes What is the mode of onset of paraplegia Acutewithin days  Transverse myelitis  Anterior spinal artery syndrome  Traumatic paraplegia Sub-acute 2- 6 weeks  Pott’s paraplegia  Spinal epidural abscess  Spinal cord tumors Chronic ˃ 6weeks  Familial spastic paraplegia  Amyotrophic lateral sclerosis  Cranio-vertebral junction anomalies

Legend First-order neuron Second-order neuron Third-order neuron Pain stimulus Lesion Sensory impairment Function intact Function lost Light touch stimulus

Lesion of the right dorsal column at L1 produces what impairment? Damage to the right dorsal column at L1 causes the absence of light touch, vibration, and position sensation in the right leg. Only fasciculus gracilis exists below T6. RL

Lesion of the right fasciculus cuneatus at C3 produces what impairment? Damage to the right fasciculus cuneatus at C3 causes the absence of light touch, vibration, and position sensation in the right arm and upper trunk. RL

Right Fasciculus Cuneatus Lesion Fasciculus cuneatus lesion Ipsilateral loss of light touch, vibration, and position sense In the right arm and upper trunk RL DRG C3 Common causes include MS, penetrating injuries, and compression from tumors.

Lesion of the right lateral corticospinal tract at L1 produces what impairment? Damage to the right lateral corticospinal tract at L1 causes upper motor neurons signs (weakness or paralysis, hyperreflexia, and hypertonia) in the right leg. RL

R L UMN Lateral corticospinal tract lesion Ipsilateral UMN signs below the lesion level Weakness (Spastic paralysis) Hyperreflexia (+ Babinski, clonus) Hypertonia Right Lateral Corticospinal Tract Lesion L1 Common causes include penetrating injuries, lateral compression from tumors, and MS.

Damage to the right lateral spinothalamic tract at L1 causes the absence of pain and temperature sensation in the left leg. Lesion of the right lateral spinothalamic tract at L1 produces what impairment? R L

R L DRG Lateral spinothalamic tract lesion Contralateral loss of pain and temperature sense Right Lateral Spinothalamic Tract Lesion L1 Common causes include MS, penetrating injuries, and compression from tumors.

Damage to the anterior gray and white commissures at C5-C6 causes the absence of pain and temperature sensation in the C5 and C6 dermatomes in both upper extremities. Lesion of the anterior gray and white commissures (central cord syndrome) at C5-C6 produces what impairment? RL

C5-C6 Central Cord Syndrome Lateral Spinothalamic Tract Impaired pain and temperature sensation, C5-C6 dermatomes, bilaterally DRG R L Common causes include posttraumatic contusion and syringomyelia, and intrinsic spinal cord tumors.

Postraumatic central cord syndrome MRI of the cervical spine focal posterior disc protrusion at C3/4 level causing spinal stenosis obliterating CSF space and impressing onto the spinal cord. There is increased intramedullary T2 signal without abnormal T1 signal noted

Damage to the right dorsal columns at L1 causes the absence of light touch, vibration, and position sense in the right leg. Damage to the lateral corticospinal tract causes upper motor neuron signs in the right leg (Monoplegia), and damage to the lateral spinothalamic tract causes the absence of pain and temperature sensation in the left leg. Complete transection of the right half the spinal cord (Hemicord or Brown-Sequard syndrome) at L1 produces what impairments? RL

RL Hemicord Lesion (Brown-Sequard Syndrome) Dorsal column lesion Ipsilateral loss of light touch, vibration, and position sense Lateral corticospinal tract lesion Ipsilateral upper motor neurons signs Lateral spinothalamic tract lesion Contralateral loss of pain and temperature sense Hemicord lesion L1 Common causes include penetrating injuries, lateral compression from tumors, and MS.

Hemicord Lesion (Brown-Sequard Syndrome) Cervical spine MRI showing a T2 hyperintense enhancing lesion at C2-3

Damage to the dorsal columns, bilaterally, causes the absence of light touch, vibration, and position sense in the both legs. Damage to the lateral corticospinal tracts, bilaterally, cause upper motor neuron signs in the both legs (Paraplegia), and damage to the lateral spinothalamic tracts, bilaterally, cause the absence of pain and temperature sensation in the both legs. Complete transection of the spinal cord (Transverse cord lesion) at L1 would produce what impairments? RL

RL Dorsal column lesion Bilateral loss of light touch, vibration, and position sense Lateral corticospinal tract lesion Bilateral upper motor neurons signs Lateral spinothalamic tract lesion Bilateral loss of pain and temperature sense Transverse Cord Lesion Transverse cord lesion Common causes include trauma, tumors, transverse myelitis, and MS.

An MRI showing a Transverse myelitis lesion (the lesion is the lighter, oval shape at center-right), this MRI was taken 3 months after patient recovered

Clinical approach to Spinal cord syndromes Clinical features anterior, central, Brown- Séquard syndrome Anterior spinal cord syndrome is usually seen as a result of compression of the ASA. Sensory loss is incomplete. Sensitivity to pain and temperature are lost while sensitivity to vibration and position are preserved. Central cord syndrome is results impairment in the arms and hands and to a lesser extent in the legs. Loss of fine control of movements in the arms and hands, relatively less impairment of leg movements. Loss of bladder control may also occur, as well as painful parethesia. Brown-Séquard syndrome is a loss of sensation and motor function (paralysis and anesthesia) that is caused by the lateral hemisection (cutting) of the spinal cord.

Damage to the lateral corticospinal tracts cause upper motor neuron signs, bilaterally, below the lesion level. Damage to lower motor neurons in the ventral horns cause lower motor neuron signs, bilaterally, at the lesion level. Damage to the lateral spinothalamic tracts cause absence of pain and temperature sensation, bilaterally, below the lesion level. Sparing of the dorsal columns leaves light touch, vibration, and position sense intact throughout. Complete transection of the lateral corticospinal and lateral spinothalamic tracts with sparing of the dorsal columns, bilaterally, (anterior cord syndrome) in the cervical region would produce what impairments? RL

UMN DRG UMN DRG R L Anterior cord lesion Lateral corticospinal tract lesion Ipsilateral upper motor neurons signs Contralateral loss of pain and temperature sense Lateral spinothalamic tract lesion Anterior Cord Syndrome Common causes include anterior spinal artery infarct, trauma, and MS.

Left: hyperintense intramedullary lesion in T2 at the level C3-C7 (arrows), indicate acute cervical spinal cord infarction. Right: MR sagittal T2: myelomalacia cavity C3-C7 in control after a month. Anterior Cord Syndrome

R L Posterior Cord Syndrome DRG Dorsal column lesion (bilateral) Bilateral loss of light touch, vibration, and position sense, generalized below lesion level Common causes include trauma, compression from posteriorly located tumors, and MS.

Posterior Cord Syndrome

Damage to the dorsal columns (fasciculus gracilis and cuneatus), bilaterally, causes the absence of light touch, vibration, and position sense, bilaterally, from the neck down (below the lesion level). Complete transection of the dorsal columns, bilaterally, (posterior cord syndrome) in the cervical region would produce what impairments? RL