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Spinal Cord

Important Points:


  1. It extends from the foramen magnum in the skull to the lower border of first lumbar vertebrae. Q
  2. Filum terminale – A fibrous extension of conus medullaris that terminates at the coccyx. Q
  3. iConus medullaris – Below lumbar enlargement the spinal cord narrow and ends as conus medullaris.
  4. Cauda – equina – The lumbar roots from L2 and sacral roots congregate around the filum terminale and form cauda. equina.
  5. Cervical enlargement C5 – T1, widest at C6 – Due to formation of brachial plexus.
  6. Lumbar enlargement L3 – S2 widest at S1 – Due to formation of lumbosacral plexus.

Blood Supply

  1. Spinal cord is supplied by one ant. spinal artery (ant. 2/3) and a pair of post. Spinal arteries (post 1/3)

Table 377-2 Spinal Cord Levels Relative to the Vertebral Bodies
(Ref. Hari. 18th ed., Pg- 3366)


Spinal Cord Level

Corresponding Vertebral Body

Upper cervical

Same as cord level

Lower cervical

1 level higher

Upper thoracic

2 levels higher

Lower thoracic

2 to 3 levels higher





Sensations Transmitted by Posterior/Dorsal Column

  1. Fine Touch (Sensations requiring fine gradients of intensity/high degree of localization)
  2. Fine Pressure (Fine degrees of judgment of pressure intensity)
  3. Vibration
  4. Joint Position Sense

Sensations Transmitted by Anterolateral Column/Spinothalamic Tract

  1. Crude Touch                
  2. Crude pressure
  3. Pain (Pin Prick)            
  4. Temperature
Important Point:

Fine touch are transmitted by the Posterior column.

Spinal cord had 31 pairs of spinal nerves.Q


Vertebral column

Spinal cord segment

Lower cervical

Add 1

T1 – T6

Add 2

T7 – T9

Add 3


L1 – L2


L3 – L4




Sacral & coccygeal

Segmental levels of some common reflexes include:





Ankle jerk : S1, S2

Knee jerk: L3,4

Biceps jerk: C5, 6

Triceps jerk : C 7,8

Radial jerk : C 6

Jaw Jerk : Pons

Plantar reflex : S1, S2

Abdominal reflex : T7 - T11 Cremasteric reflex : L1

Beevor’s sign
  1. It is characteristic of spinal cord injury between T6 and T10 levels.
  2. This occurs because the upper abdominal muscle such as the Rectus Abdominus are intact at the top of the abdomen but weak at the lower portion. Thus when the patient is asked to do a sit up only the upper muscles contract pulling the umbilicus toward the head in patients who are abnormal.
  3. It is also seen in amyotrophic lateral sclerosis and facioscapulohumeral muscular dystrophy.

Brown Séquard syndrome

Brown Séquard syndrome (Hemisection of the cord)

  1. Sensations lost on the same side as the lesion (Ipsilateral posterior column involvement)
    1. Vibration
    2. Joint Position (Proprioception)
    3. Fine touch
  2. Motor power is lost on the same side as that of the lesion (Ipsilateral corticospinal tract involvement)
  3. Sensation lost on the opposite side of lesion (Contralateral spinothalamic tract involvement).
    1. Touch (Crude touch)
    2. Pain
    3. Temperature

Diseases Involving Spinal Cord

  1. Spinal cord compression       
    1. Cervical spondylosis                             
    2. Cervical or thoracic disc
    3. Metastatic tumor                          
    4. Primary tumor (meningioma, neurofibroma etc)
    5. Infective (epidural abscess, spinal TB etc)    
    6. Epidural haematoma
  2. Inflammatory disorders
    1. Multiple sclerosis
    2. Idiopathic transverse myelitis
    3. Sarcoidosis
    4. Infections (lyme, zoster, TB, AIDS)
  3. Degenerative disorders
    1. Motor neuron disease
    2. Syringomyelia
  4. Vascular      
    1. Spinal cord infarction
    2. Vasculitis, systemic lupus erythematosus etc
    3. Spinal AVM
  5. Trauma Metabolic/Nutritional
    1. Cord contusion, laceration or transaction
    2. Displaced vertebral fracture or disc
    3. Traumatic epidural haematoma
  6. B12 deficiency (subacute combined degeneration)
  7. Rare hereditary conditions
    1. Friedreich ‘s ataxia Hereditary spastic paraparesis
  8. Parasagittal brain lesions
    1. Meningioma
    2. Cerebral venous sinus thrombosis


  1. Syringomyelia is a developmental cavity of the cervical cord that is prone to enlarge and produce progressive myelopathy.
  2. Many young patients acquire a cervical-thoracic scoliosis. More than half of all cases are associated with Chiari type 1 malformations in which the cerebellar tonsils protrude through the foramen magnum and into the cervical spinal canal.
  3. Acquired cavitations of the cord in areas of necrosis are also termed syrinx cavities; these follow trauma, myelitis, necrotic spinal cord tumors, and chronic arachnoiditis due to tuberculosis and other etiologies.
  4. The presentation is a central cord syndrome consisting of dissociated sensory loss (loss of pain and temperature sensation with sparing of touch and vibration) (‘Dissociate Anaesthesia’ and is considered as the “True Hallmark of the disease”.) and areflexic weakness in the upper limbs.
  5. The sensory deficit has a distribution that is "suspended" over the nape of the neck, shoulders, and upper arms (cape distribution) or in the hands.
  6. Muscle wasting in the lower neck, shoulders, arms, and hands with asymmetric or absent reflexes in the arms reflects expansion of the cavity into the gray matter of the cord.
  7. As the cavity enlarges and further compresses the long tracts, spasticity and weakness of the legs, bladder and bowel dysfunction, and a Horner's syndrome appear.
  8. Some patients develop facial numbness and sensory loss from damage to the descending tract of the trigeminal nerve (C2 level or above).
  9. In cases with Chiari malformations, cough-induced headache and neck, arm, or facial pain are reported. Extension of the syrinx into the medulla, syringobulbia, causes palatal or vocal cord paralysis, dysarthria, horizontal or vertical nystagmus, episodic dizziness or vertigo, and tongue weakness with atrophy.
  10. MRI scans accurately identify developmental and acquired syrinx cavities and their associated spinal cord enlargement.

Treatment: Syringomyelia

  1. Treatment of syringomyelia is generally unsatisfactory.
  2. The Chiari tonsillar herniation is usually decompressed, generally by suboccipital craniectomy, upper cervical laminectomy, and placement of a dural graft. 
  3. Syringomyelia secondary to trauma or infection is treated with a decompression and drainage procedure in which a small shunt is inserted between the syrinx cavity and the subarachnoid space; alternatively, the cavity can be fenestrated.

Anterior spinal Artery Thrombosis/Syndrome

  1. Anterior Spinal Artery is a single artery that supplies the anterior two thirds of the spinal cord.
  2. Sparing of posterior column
    Posterior 1/3” of the cord is supplied by the posterior spinal artery and hence the posterior column is spared and vibration & joint position sense are preserved
  3. Pain at site of infarction
    Moderate to severe back pain at the site of cord infarction, most often in the thoracic region.
  4. Infarction of the corticospinal tract
    1. Paraplegia with UMN signs (Spasticity and hyper-reflexa)
      Note: That initially flaccidity and hyporeflexia may be seen in patients is in of spinal shock
  5. Infarction of the anterolateral tracts (spinothalamic tract)
    1. Loss of pain and temperature sensation distal to the lesion
  6. Infarction of the fibres required for sphincter control (carried in anterior 2/3rd of cord)
    1. Loss of bladder control

Spinal cord compression

Table: Causes of spinal cord compression.





Vertebral (Extradural)


Trauma, Intravertebral disc prolapse,

Secondary from Breast, Prostate, Bronchus,

Myeloma, Tuberculosis

Meninges Intradural (extramedullary)


Tumours, Meningioma, Neurofibroma, Ependymoma, Metastasis, Lymphoma, Leukaemia,

Epidural abscess

Spinal cord (intradural intramedullary)



Glioma, Ependymoma, Metastasis

Lesions at various sites of spinal cord

  1. Above the fifth cervical segment – upper motor neurone signs and sensory loss of all four limbs;
  2. Between fifth cervical and first thoracic – lower motor neurone signs and segmental sensory loss in the arms and upper motor neurone signs in the legs;
  3. Thoracic cord – spastic paraplegia with a sensory level on the trunk;
  4. Lumbosacral cord and cauda equina – lower motor neurone signs and segmental sensory loss in the legs. The spinal cord ends at approximately the T12/L1 spinal level and spinal lesions below this level can only cause lower motor neuron signs.
  5. The Brown-Séquard Syndrome results if damage is confined to one side of the cord. On the side of the lesion there is a band of hyperesthesia with below it loss of proprioceptive sense and upper motor neurone signs. On the other side there is loss of spinothalamic sensation (pain, temperature) as fibers of that tract decussate soon after entering the cord.

Comparison of intramedullary and extramedullary Compression

1. Symptoms



a. Root pain



b. Vertebral pain



c. Muscle Weakness



d. Sacral Involvement




2. Signs



a. Brown Séquard



b. Dissociative sensory loss



c. Bladder/ bowel dysfunction




3. Investigation –



Subarachnoid Block

Late & less marked

Early & marked

Extramedullary Spinal Cord Compression:


Acute and chronic conditions characterized by external mechanical compression of the SPINAL CORD due to extramedullary neoplasm; EPIDURAL ABSCESS; SPINAL FRACTURES; bony deformities of the vertebral bodies; and other conditions.

Clinical manifestations vary with the anatomic site of the lesion and may include localized pain, weakness, sensory loss, incontinence, and impotence.

A Hoffmann (or Tinel's sign) is a tingling sensation triggered by a mechanical stimulus in the distal part of an injured nerve. This sensation radiates peripherally, from the point where it is triggered to the cutaneous distribution of the nerve. The tingling response can be compared with that produced by a weak electric current, as in transcutaneous electrical nerve stimulation (TENS). This unpleasant sensation is not a severe pain and does not persist

Different between conus medullaris and Cauda Equina



Conus medullaris

Cauda equina

1. Root involved

S3, S4, S5,


2. Root pains

- uncommon


3. Involvement

- B/L


4. Symmetry

- Symmetrical


5. Site

- Perineum


6. Motor Signs

- Usually no weakness

Weakness below knee, Asymmetric weakness

7. Knee reflex

- Present


8. Ankle reflex

- Absent


9. Sensory-

- Dissociated anesthesia (LQ 2012)

No dissociation

10. Bladder/bowel

- Early & marked (LQ 2012)

Late, less marked

Note: Conus medullaris syndrome is a very important DD of BHP. But in BHP there is no loss of peri anal sensation and ankle jerk is normal.

Causes of spastic paraplegia

  1. Cervical spinal cord injury
  2. Decompression sickness
  3. Infectious Disorders (Specific Agent)
    1. HIV             
    2. Syphilis
    3. Potts paraplegia/Epidural cold abscess          
    4. Tabes dorsalis
  4. Infected organ, Abscesses
    1. Spinal epidural abscess
  5. Neoplastic Disorders
    1. Cervical/Thoracic spinal cord tumor    
    2. Metastasis to spinal cord
    3. Intraspinal tumor                 
    4. Spinal Meningioma               
    5. Multiple Sclerosis
  6. Deficiency Disorders
    1. Copper deficiency                
    2. Vitamin B12 deficiency (Subacute combine degeneration)
  7. Congenital, Developmental Disorders
    1. Congenital narrow neural canal/Cervical               
    2. Syringomyelia
  8. Hereditary, Familial, Genetic Disorders
    1. Hereditary spastic Paraplegia       
    2. Friedreich’s ataxia       
    3. Hereditary Spinocerebellar ataxia type I
  9. Anatomic, Foreign Body, Structural Disorders
    1. Spondylosis, cervical                
    2. Cervical spinal stenosis
    3. Parasaggital Brain Lesion
  10. Drugs
    1. Nitrous oxide (N2O) Administration/Toxicity/abuse
  11. Poisoning (Specific Agent)
    1. Lathyrism
Note: In lead poisoning it resembling radial neuropathy, ANP & blue line in gum (Burton lines)
Important Points:

Transverse Myelitis


Acute/subacute generally monophasic, inflammatory disorder of the spinal cord.



  1. Immunological – Post infections – Influenza, measles, varicella, rubella, mumps, EBV, CMV,
    Post vaccine – rabies, influenza
  2. Demyelination – Multiple Sclerosis
  3. Connective tissue disorders – SLE, Sjögren’s syndrome, Beh|et’s disease, sarcoidosis.
    1. Diagnostic criteria –
      1. Acute/Subacute onset                        
      2. Motor, Sensory & Sphincter disturbances
      3. Truncal sensory level                        
      4. No clinical/ lab evidence of cord compression
      5. Absence of other known neurological disease    
      6. Lack of progression over 4 weeks
    2. Clinical features
      1. Most common site upper/ mid thoracic cord
      2. Initial symptom focal back pain/ neck pain.
      3. Paresthesia, sensory, motor, sphincter disturbances with in hours to days.
      4. Areflexia initially → Hyperreflexia.
        CSF – Pleocytosis, Proteins mildly increase.
    3. Poor prognosis –
      1. Spinal shock
      2. Severe back pain
    4. Treatment – I.V. Methyl Prednisolone followed by oral prednisolone.

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