Clinical localisation of spinal cord disorders.

We discussed spinal cord anatomy and various spinal cord syndromes in the last session. We will use that knowledge to localise spinal cord lesions in this session. The spinal cord lesions have an axial and vertical localisation. Axial localisation refers to whether a lesion is intramedullary or extramedullary. Transverse myelitis is a classic example of an intramedullary lesion. Cervical spondylosis with myelopathy is an example of an extramedullary compressive lesion. Vertical localisation refers to the lesion being in the cervical, thoracic, lumbar or sacral level and within each, which segmental level. For example, a patient with paraplegia and sensory level at T10 with Beevor’s sign positive localise the lesion to the thoracic cord, T10 level.

Axial localisation.

Axial localisation refers to whether the lesion is intramedullary, i.e. within the spinal cord, or extramedullary, i.e. lying outside the spinal cord. The extramedullary lesions can be further divided into extradural and intradural depending on whether the lesion is inside or outside the dura. Cervical spondylosis with myelopathy is an example of an extradural extramedullary lesion. A meningioma compressing the cord is an example of an intradural extramedullary lesion. It is difficult to differentiate between intradural and extradural extramedullary lesions. The presence of vertebral pain and tenderness, deformity like a step or gibbus in the back are the clues to distinguish between the two.

An extramedullary compressive lesion goes through three stages, according to Oppenheim. An initial stage of radicular pain and segmental motor and sensory symptoms. The initial phase is followed by a Brown-Sequard syndrome and finally a complete transection of the cord. The rapidity of development of these stages depends on the aetiology and can be acute or chronic. Some of the cardinal features of extramedullary compression include Radicular or root pain, which is a unilateral lancinating pain down the dermatome on coughing, straining, or Valsalva. The patient will have early corticospinal tract involvement with lower limb spasticity more than the upper limb. The leg is more involved as leg fibres are laterally placed in the corticospinal tract than arm fibres. The LMN findings are rare and, if present, occur at the segmental level at the site of compression. The patient will have only late bladder involvement. They have ascending paresthesia as sacral fibres are laterally placed in the spinothalamic tract. Funicular or tract pain is less common. The patient can have vertebral pain and tenderness, which suggest extramedullary extradural lesion.

The intramedullary lesion arises within the spinal cord. It can present as a central cord syndrome, like syringomyelia or complete transection of the cord as in transverse myelitis. It can be patchy, short segment or long segment. All intramedullary lesions share some common features, which include early bladder involvement except in the case of syringomyelia. Lower motor neuron weakness is more prominent due to early anterior horn cell involvement. Upper motor neuron weakness and signs are late. Radicular pain and vertebral pain are rare in an intramedullary lesion. Tract or funicular pain is more common. Descending paresthesia and sacral sparing are seen as sacral fibres are laterally placed in the lateral spinothalamic tract and are the last to involve in an intramedullary lesion.

All findings may not be present in an individual case. There may be some overlap between intramedullary and extramedullary features. Imaging will be required to differentiate between the two in some cases.

Vertical localisation.

The patient will have a weakness level, reflex level and sensory level. The history, along with these three levels, helps to localise the lesion in the spinal cord properly. The sensory level is most helpful in a thoracic cord lesion with minimal dermatomal overlap. It is important to remember that the pain and temperature fibres cross over to the opposite side only two segments above the entry level. It can produce localisation confusion in Hemi-cord transection. The sensory level is less reliable in cervical and lumbar spinal cord lesions due to the significant dermatomal overlap. Here the reflex level is more helpful in localisation as the reflex will be sluggish or absent at the lesion level and exaggerated below the lesion level. The patient will have lower motor neuron findings, including hypotonia, decreased reflexes, weakness and wasting at the level of the lesion and upper motor neuron findings below the lesion. For example, in a patient with cervical myelopathy due to spondylosis at the C5 level. The biceps and supinator reflex will be absent. The triceps and finger flexors are exaggerated. The patient may not have a proper sensory level due to the significant overlap of dermatomes in the upper limb.

Now let us learn some specific findings at certain levels. It is important to remember that all findings may not be present in an individual case. The absence of a sign does not take anything away from diagnosis if other features are corresponding. For example, In a patient with a T10 segment lesion, the presence of the Beevor sign will help to localise the lesion. The same patient can also present without the Beevor sign. The absence of the Beevor sign does not rule out the possibility of a T10 lesion. If it is there, it helps. If it is not there, still the localisation is possible. You don’t have to give an explanation for a normal finding, which is the absence of Beevor, in a patient with a T10 lesion.

Foramen magnum lesion

Foramen magnum lesion causes high cervical myelopathy. The findings in a foramen magnum lesion include neck stiffness, down beating nystagmus and papilledema due to CSF obstruction. The patient can have a facial sensory loss in an onion skin pattern due to the involvement of the long tract of the trigeminal nucleus extending to the cervical cord. Lower cranial nerve palsy can occur due to the extension of the lesion to the brainstem. A ’round the clock’ upper motor neuron weakness can occur with weakness spreading from the ipsilateral upper limb to the ipsilateral lower limb. Then the contralateral lower limb will be involved, and finally, the contralateral upper limb. They can have an atypical presentation. At the pyramidal decussation, the segregation of arm fibres occur rostrally and leg fibres caudally. A lesion can cause an unusual weakness involving the ipsilateral lower limb and contralateral upper limb. This is called Hemiplegia cruciate. The patient can have suboccipital pain in the C2 dermatome. The patient can also have Lhermitte’s sign which is an electric shock-like sensation transmitted down the spine or to the extremities with sudden flexion of the neck. The common causes for foramen magnum lesions include tumours like meningioma, atlantoaxial dislocation, basilar invagination etc.

High cervical lesion C1-C4

Along with quadriparesis, these patients will have weakness of the sternocleidomastoid and trapezius as the spinal portion of the spinal accessory nerve is involved. They may have diaphragmatic palsy due to phrenic nerve involvement in C3-5 lesions. All reflexes are exaggerated. They may have sensory impairment of the entire body from C2 downwards.

C5, C6 lesions

Biceps and brachioradialis reflex innervated by C5, C6 are sluggish or absent. Triceps, finger flexor and lower limb reflexes are exaggerated. Lesions at the C5 segment alone produce inversion of brachioradialis reflex. Tapping on the radius produces exaggerated finger flexion without flexion and supination at the elbow. The patients will have LMN weakness of the Deltoid, Biceps and other C5, C6 innervated muscles. There will be UMN weakness below C5, C6 levels. In the pure C6 lesion, the lateral arm sensation is spared. The sensation of the rest of the body below it will be affected.

C7 lesion

The triceps reflex, innervated by C7, C8 roots, is sluggish or absent. The Biceps and brachioradialis reflexes are normal. The patient may have a paradoxical triceps reflex, which is flexion of the forearm on tapping olecranon due to contraction of normal biceps and absent triceps reflex. The finger flexor reflex is exaggerated. The patient will have weakness of flexors and extensors of the wrist. They may have a sensory loss at and below the 3rd and 4th digits.

C8, T1lesions

The patient may have unilateral or bilateral Horner’s syndrome. They will have weakness and wasting of small muscles of the hand along with spastic paraparesis. The finger flexor reflex will be absent. They may have sensory loss over the 5th digit, medial forearm, arm and rest of the body below it.

Thoracic cord lesion.

The patient will have spastic paraplegia with a reliable sensory level mostly. The nipple corresponds to the T4 level, and the umbilicus corresponds to T10. The patient may have root pain that mimics intercoastal neuralgia. Most patients will have bladder, bowel and sexual dysfunction. The patient’s with lesions above T5 may have postural giddiness due to sympathetic dysfunction. Autonomic dysreflexia is a feature of thoracic cord lesion above T6 characterised by hypertension, excessive sweating and reflex bradycardia precipitated by small stimuli like a distended bladder. The superficial abdominal reflex helps in localising lower thoracic cord lesions. All reflexes are absent in the T6 lesion. Upper superficial abdominal reflex spared in T10 lesion. Both upper and lower superficial abdominal reflexes are normal in T12 lesions. In the T10 lesion, the Beevor’s sign is positive. The normal upper abdominal muscle pulls the umbilicus upwards when the patient flexes the head in the supine position.

L1 lesion.

The patient will have spastic paraparesis. The lower abdominal muscles are weak but challenging to demonstrate clinically. The Knee and ankle jerks are brisk. There will be sensory loss below the groin in both lower limbs.

L2, L3, L4 Lesion.

In the L2 lesion, the cremasteric reflex is absent. In L2, L3, L4 lesions, the knee jerk is sluggish or absent. The ankle jerk is brisk. Sensory over the front of the thigh is spared in pure L4 lesion.

L5 lesion

The extensor hallucis longus and foot dorsiflexion are weak. The hip flexion, adduction and knee extension are normal. The knee jerk is normal. The ankle jerk is hyperactive. The sensation is normal in the thigh, medial side of the leg, foot and sole. It is impaired from the L5 dermatome downward.

S1, S2 lesion

The patient will have weakness of plantarflexion and foot muscles. The ankle jerk is absent. The knee jerk is normal. There is loss of sensation in the sole of feet, heel, outer aspect of foot and ankle. The posterior thigh and saddle area is also anaesthetic.

The spinal cord segments from L4-S2 is also called the epiconus. The lesion involving these segments is called the epiconus syndrome.

Conus medullaris

Conus medullaris is the lower end of the spinal cord. Lesion there causes damage to S3, S4, S5 segments of the spinal cord. Clinical features include weakness of pelvic floor muscles and early bladder involvement. There will be loss of voluntary initiation of micturition and bladder sensation with increased residual urine. The patient will have constipation with impaired erection and ejaculation. The anal and bulbocavernosus reflexes are absent. They will have symmetric saddle anaesthesia. Radicular pain is absent in pure conus syndrome. Perineal pain can occur late in the course of the disease.

Cauda equina

The spinal cord ends at L1 vertebral level. The involvement of roots in the spinal canal below the L1 vertebra is called cauda equina. So, it is not a spinal cord syndrome in the real sense. Any roots from L2 to S5 may be involved often in an asymmetric pattern. It produces an asymmetrical motor sensory pure lower motor neuron syndrome. The knee and ankle jerk are variably affected. Asymmetric early radicular pain is characteristic of cauda equina syndrome. Bowel and bladder involvement is rare and usually late. It can occur in extensive lesions. Sometimes lesions can involve both conus and cauda equina, and we will get a combination of clinical findings.

We have learned how to localise a spinal cord lesion. Once you localise, check if it falls into any of the syndromes we studied in the previous session. That helps in finding the aetiology. For example, sudden paraplegia with intramedullary localisation sparing only the posterior column suggests anterior spinal artery syndrome. It helps to identify spinal cord ischemia as the probable aetiology. Now let us localise a clinical case with what we have learned in this session.

A 70-year-old head load worker presented with walking difficulty of 1-year duration. He had neck pain radiating down the right upper limb, which increased with coughing and straining. He had heaviness of both lower limbs with tipping over fine obstacles. There was slipping of chappals with knowledge from both feet. He had urinary symptoms for the last three months, including urgency and frequency. The patient had a normal higher function and cranial nerve examination on examination. Motor system examination showed spasticity of both lower limbs. There was bilateral toe grip weakness with grade 4 power in the right biceps. Biceps and brachioradialis reflexes were absent on the right side. There was an inversion of the right brachioradialis reflex with an exaggerated finger flexor reflex. Lower limb reflexes were exaggerated with extensor plantar bilaterally. The joint position sense was impaired on both lower limbs with no sensory level. Examination of the skull and spine showed tenderness over the cervical spine.

The diagnosis in neurology, as usual, contains four parts. The functional deficit in this patient is spastic quadriparesis. The anatomical localisation in the axial plane is possibly an extramedullary lesion given the radicular pain and late bladder involvement. It is most likely extramedullary extradural as the patient had tenderness over the vertebrae. The vertical localisation is in the cervical spine. The motor and reflex level here is at C5, C6. There is no sensory level in this case. Given the inversion of the brachioradialis reflex, the localisation is probably at the C5 level. The patient being a headload worker, the most probable aetiology is cervical spondylosis. The MRI cervical spine of the patient showed disc prolapse at C4-C5 and C5-C6 levels with myelomalacia in the spinal cord and compression on the exiting right C5 root. The patient was treated with surgical decompression and fixation with a near-complete resolution of symptoms. The final diagnosis of this patient is Spastic quadriparesis due to an extramedullary extradural compressive lesion on the cervical cord at C5 level due to cervical spondylosis.

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