Brown-Séquard Syndrome; Cause, Symptom, Treatment

Brown-Séquard syndrome








User Review


5
(11 votes)


Brown-Séquard syndrome is characterized by anatomical disruption of nerve fiber tracts in one half of the spinal cord. Disruption of descending lateral corticospinal tracts, ascending dorsal column and ascending spinothalamic tracts leads to ipsilateral hemiplegia and loss of proprioception and vibration with contralateral loss of pain and temperature sensation below the level of injuries. Common causes of BSS include cord trauma, neoplasms, disk herniation, demyelination, infective/ inflammatory lesions or epidural hematomas with penetrating trauma to the cord being commonest cause,. In literature, very few cases of penetrating stab cord injury presenting with pure BSS have been described. Management of BSS depends on the causative pathology. Need for conservative or surgical management depends on the patient’s neurological status and clinical-radiological findings. Surgery intervention is advised in post-traumatic BSS if there is a presence of retained foreign objects, CSF leakage, infection or signs of extrinsic spinal cord compression. Medical management is preferred for infective/ inflammatory or demyelinating causes of BSS while surgical treatment is performed for pathologies causing extrinsic cord compression,.

Brown-Séquard syndrome (also known as Brown-Séquard’s hemiplegia, Brown-Séquard’s paralysis, hemiparaplegic syndrome, hemiplegia et hemiparaplegia spinal is, or spinal hemiparaplegia) is caused by damage to one half of the spinal cord, resulting in paralysis and loss of proprioception on the same (or ipsilateral) side as the injury or lesion, and loss of pain and temperature sensation on the opposite (or contralateral) side as the lesion. It is named after physiologist Charles-Édouard Brown-Séquard, who first described the condition in 1850.

Brown-Séquard syndrome occurs due to the involvement of ipsilateral corticospinal tract and dorsal column which accounts for ipsilateral weakness and loss of proprioception and contralateral spinothalamic tract which causes contralateral loss of temperature and pin-prick sensations ().

 

What is Brown-Séquard Syndrome?

Alternative Name

  • BSS
  • Hemisection of the Spinal Cord
  • Partial Spinal Sensory Syndrome
  • Hemiparaplegic Syndrome
  • Spastic Spinal Monoplegia Syndrome

Pathophysiology

A complete Brown-Séquard syndrome with hemisection of the spinal cord seldom occurs. Hemi-section of the chord creates lesions on the following neural system –

Brown-Séquard syndrome results from damage to or loss of ascending and descending spinal cord tracts on 1 side of the spinal cord. Scattered petechial hemorrhages develop in the gray matter and enlarge and coalesce by 1-hours postinjury. Subsequent development of hemorrhagic necrosis occurs within 24-36 hours. White matter shows petechial hemorrhage at 3-4 hours. Myelinated fibers and long tracts show extensive structural damage.

  • The Corticospinal Tract – It produces spastic paralysis on the same side of the body where the lesion has occurred. The paralysis is normally detected below the lesion. At the level of the lesion, flaccid paralysis arises, which means the muscles lose their ability to move to lead to weakness or paralysis of the adjoining parts.
  • The Lateral Spinothalamic Tract –  It leads to loss of pain and temperature sensations in the contralateral (opposite) side beginning one or two segments below the point of lesion.
  • Posterior Columns – A lesion in the Gracile fasciculus or the Tract of Goll leads to loss of sense of vibration, proprioception, and soft touch in the ipsilateral side. Same symptoms are detected in case of the lesion in the Cuneate fasciculus or the Tract of Burdach.

Some associate causes are described billow

Carpal Tunnel Syndrome

  • Causes include entrapment, excessive use of the wrist, tenosynovitis, local infiltration – eg, acromegaly, amyloidosis.
  • Patients complain of nocturnal paraesthesia affecting the thumb, index and middle fingers.
  • Reduced sensation in the same area.
  • Severe cases – weakness and wasting of the abductor pollicis brevis.

Ulnar Neuropathy

  • Usually caused by a lesion at the ulnar groove or in the cubital tunnel or prolonged pressure at the base of the hand (affecting the deep branch).
  • Maybe iatrogenic following humeral fracture treatment.
  • Claw hand deformity may be seen if there is complete paralysis in the fourth and fifth fingers with wasting and weakness of small muscles of the hand. This leads to hyperextension at the metacarpophalangeal (MCP) joints and flexion at the interphalangeal (IP) joints.
  • Sensory loss over the fifth finger and the outer half of the fourth finger and palm.
  • The weakness of small muscles without sensory loss occurs if the deep palmar branch of the ulnar nerve is affected.

Thoracic Outlet Syndrome

  • Caused by compression of nerves of the brachial plexus – eg, the presence of a fibrous band or cervical rib. See the separate article on Cervical Ribs and Thoracic Outlet Syndrome.
  • Pain in the arm.
  • Paraesthesia in the arm and hand (usually in C8 and T1 distribution).
  • Atrophy of the hand.
  • The weakness of the arm.
  • Rarely, there may be cyanosis or edema of the arm.

Tarsal Tunnel Syndrome

  • Caused by ankle sprains and fractures, ill-fitting footwear, cysts, ganglia, arthritis, tenosynovitis.
  • Pain in the ankle and the sole of the foot.
  • Paraesthesia on walking.
  • Tibial nerve trunk is tender (posterior to the medial malleolus).
  • The sensory deficit on the foot.
  • The weakness of the plantar flexion.

Radial nerve compression

  • Radial neuropathy usually results from compression against the humerus.
  • Leads to ‘Saturday night palsy’.
  • Wrist and finger drop.
  • Variable paraesthesia – look for a sensory loss in the dorsal aspect at the root of the thumb.

Lateral Femoral Cutaneous Nerve Compression

  • Leads to meralgia paraesthetica.
  • Numbness in the lateral aspect of the thigh.
  • Severe pain which restricts activities (reproduced by palpation under the anterior superior iliac spine).
  • Paraesthesia in the anterolateral aspect of the thigh.
  • No motor weakness.

Sciatic Nerve Damage

  • Sciatic nerve damage can result from fractures of the pelvis or femur or from pelvic tumors.
  • Paraesthesia over the lateral aspect of the leg below the knee.
  • The weakness of the hamstring and all muscles below the knee.

Common peroneal nerve

  • Caused by trauma or surgery.
  • Leads to foot drop.
  • Weakness on the everting foot.
  • Inability to extend the toes.
  • Paraesthesia over the dorsum of the foot.

Single neuropathies affecting the thoracodorsal, dorsal scapular, suprascapular and medial pectoral nerves have been described in bodybuilders. Other mononeuropathies include Bell’s palsy, interosseous nerve compression and femoral nerve entrapment.

An apparent mononeuropathy may be the presenting feature of a peripheral neuropathy.

Causes of Brown-Séquard syndrome 

Traumatic causes

  • Brown-Séquard syndrome can be caused by any mechanism resulting in damage to 1 side of the spinal cord. Multiple causes of Brown-Séquard syndrome have been described in the literature. The most common cause remains traumatic injury, often a penetrating mechanism, such as a stab or gunshot wound or a unilateral facet fracture and dislocation due to a motor vehicle accident or fall. 
  • More unusual etiologies that have been reported include assault with a pen, removal of a cerebrospinal fluid drainage catheter after thoracic aortic surgery, and injury from a blowgun dart.  Traumatic injury may also be the result of blunt trauma or pressure contusion.

Nontraumatic causes

Numerous nontraumatic causes of Brown-Séquard syndrome have also been reported, including the following:

  • Tumor (primary or metastatic)
  • Disk herniation
  • Herniation of the spinal cord through a dural defect (idiopathic or post-traumatic)
  • Epidural hematoma
  • Vertebral artery dissection
  • Transverse myelitis
  • Radiation
  • Type II decompression sickness
  • Intravenous drug use
  • Ossification of the ligamentum flavum
  • Meningitis
  • Empyema
  • Herpes zoster
  • Herpes simplex
  • Syphilis
  • Ischemia
  • Hemorrhage – Including spinal subdural/epidural and hematomyelia

Brown Sequard Syndrome Symptoms, Signs

  • Persons with Brown Sequard Syndrome will manifest the following symptoms:
  • Interruption of the lateral corticospinal tracts
    • Ipsilateral spastic paralysis below the level of the lesion
    • Babinski sign ipsilateral to the lesion
    • Abnormal reflexes and Babinski sign may not be present in acute injury.
  • Interruption of the posterior white column:
    • Ipsilateral loss of tactile discrimination, vibratory, and position sensation below the level of the lesion
  • Interruption of lateral spinothalamic tracts:
    • Contralateral loss of pain and temperature sensation. This usually occurs 2-3 segments below the level of the lesion.
  • Temperature sensation deficit
  • Contralateral pain
  • Ipsilateral hemiplegia or half of the body is paralyzed
  • Loss of sensation of half of the body or hemianesthesia
  • Babinski sign
  • Abnormal reflexes
  • Loss of vibration
  • Horner’s syndrome
  • Sphincter disturbances
  • Loss of position sense
  • Loss of tactile discrimination

According to various symptoms of BSS are listed below:

  • Clonus
  • Babinski sign
  • Hemiparaplegia
  • Hemianesthesia
  • Loss of vibration
  • Abnormal reflexes
  • Horner’s syndrome
  • Loss of position sense
  • Ipsilateral hemiplegia
  • Increased deep reflexes
  • Sphincteral disturbances
  • Thermanesthesia below lesion
  • The sensory loss at the level of the lesion
  • Reduced tactile discrimination abilities
  • Segmental atrophy at the level of the lesion
  • Contralateral analgesia below the lesion
  • Increased muscle tone around the side of the lesion
  • Paralysis of the voluntary muscles below the level of the lesion

Diagnosis of Brown-Séquard Syndrome

On inspection, note the following:

  • The resting posture. Note whether there is unusual rotation or clawing of the hand and whether the patient is symmetrical.
  • Look for muscle wasting or hypertrophy. Note whether it is focal or diffuse.

Look for involuntary movements such as tremor, tics, myoclonic jerks, chorea or athetosis.

  • Temperature sensation deficit
  • Contralateral pain
  • Ipsilateral hemiplegia or half of the body is paralyzed
  • Loss of sensation of half of the body or hemianesthesia
  • Babinski sign
  • Abnormal reflexes
  • Loss of vibration
  • Horner’s syndrome
  • Sphincter disturbances
  • Loss of position sense
  • Loss of tactile discrimination persons with having Brown Sequard Syndrome with the interruption of the white posterior column, the person will be able to experience an Ipsilateral or on the same side of the loss of vibratory, sense of position and tactile discrimination.
  • Meanwhile, when there is an interruption of the spinothalamic lateral tracts, the person will experience the loss of the sensation under the temperature and the loss of pain.
  • Look for muscle fasciculation (sign of lower motor neuron disease process). These are subcutaneous twitches over a muscle belly at rest. Tapping the belly may stimulate fasciculation.
  • Examination of the upper limbs may be performed more easily with the patient sitting in a chair or standing.

Examination of each of the sensory modalities:

Light touch

  • Use the light touch of a finger, a piece of cotton wool or a piece of tissue paper.
  • It is important to touch and not to stroke, as a moving sensation, such as rubbing and scratching, is conducted along pain pathways.
  • Ask the patient to close their eyes and tell you when they feel you touching them.
  • Compare each limb in the same position.
  • Keep the timing of each touch irregular to avoid anticipation by the patient.
  • A logical progression is required. You may want to start testing over the shoulder and to move along the lateral aspect of the arm and up the medial side, as this moves progressively from C4 to T3 dermatomes.
  • Note any areas of hypoaesthesia or dysaesthesia.

Sharp touch (pinprick)

  • Test using a dedicated disposable pin. A disposable hypodermic needle is too sharp.
  • Use the sternal area to establish a baseline for sharpness before you begin.
  • Follow the same progression as with light touch with the patient’s eyes closed, comparing both upper limbs.
  • Ask the patient to report hypoaesthesia (feels blunter) or hyperaesthesia (feels sharper).

Temperature

  • This is often overlooked but it can be important.
  • An easy and practical approach is to touch the patient with a tuning fork as the metal feels cold.
  • Compare the quality of temperature sensation on arms, face, trunk, hands, legs, and feet.
  • Containers of warm and cool water may be used for a more accurate assessment. Ask the patient to distinguish between warm and cool on different areas of the skin with their eyes closed.

Joint position sense (proprioception)

  • Test at the distal interphalangeal joint of the index finger.
  • Hold the middle phalanx with one thumb and finger and hold the medial and lateral sides of the distal phalanx with the other. Move the distal phalanx up and down, showing the patient the movement first.
  • Ask the patient to close their eyes and move the distal phalanx up and down randomly. Ask the patient to tell you the direction of the movement each time.
  • Test on both hands.
  • If there is an abnormality, move back to the proximal interphalangeal joint and so on until joint position sense is normal.

Vibration Sense

  • Use a 128 Hz tuning fork and ensure the tuning fork is vibrating.
  • Place it on the sternum to start with so that the patient can feel the sensation.
  • Then place it on one of the distal interphalangeal joints of one of the fingers.
  • If no vibration is sensed, move backward to the metacarpophalangeal joint, the wrist, etc.
  • Asking the patient to tell you when the tuning fork stops vibrating can be helpful if there is a doubt that their vibration sense is intact.

Two-point discrimination

  • There are specific two-point discriminators available. If you don’t have one, use a paper clip that you can open out.
  • Ask the patient to close their eyes.
  • Take the patient’s index finger in one of your hands.
  • Using the discriminator or paper clip, touch the pulp of the finger with either one or two of the testing tips.
  • The patient must tell you whether they can feel one or two stimuli.
  • Find the minimum distance at which they can discriminate the two tips. Normal is at 3-5 mm.
  • Compare both index fingers and repeat for both thumbs.

Tone

  • This is the resistance felt when a joint is moved passively through its normal range of movement.
    • Ask the patient to let their shoulders and arms ‘go floppy’.
    • Flex and extend their shoulder passively and feel for abnormality of tone.
    • Repeat for the elbow and wrist.
  • Hypertonia is found in upper motor neuron lesions; hypotonia is found in lower motor neuron lesions and cerebellar disorders.
  • Cogwheel rigidity may be found in Parkinson’s disease.

Power

  • A robust assessment of power is required.
  • The Medical Research Council (MRC) has a recommended grading system for power (see table). It has been shown to have good reliability. Some express doubts over the wide range of grade 4.
  • Ask the patient to contract the muscle group being tested and then you as the examiner try to overpower that group.

Test the following

  • Abduction, adduction, flexion, and extension of the shoulder.
  • Flexion and extension of the elbow.
  • Flexion and extension of the wrist.
  • Supination and pronation of the forearm.
  • Extension of the fingers at the metacarpophalangeal and interphalangeal joints.
  • Flexion, extension, adduction, and abduction of the fingers and thumbs.
MRC scale for muscle power
0No muscle contraction is visible.
1Muscle contraction is visible but there is no movement of the joint.
2Active joint movement is possible with gravity eliminated.
3Movement can overcome gravity but not resistance from the examiner.
4The muscle group can overcome gravity and move against some resistance from the examiner.
5Full and normal power against resistance.

The wound healed uneventfully. Muscle strength was rated according to 0–5 Lovett score [] as follows:

  • 1/5: muscle flicker, but no movement
  • 2/5: movement possible, but not against gravity
  • 3/5: movement possible against gravity, but not against resistance by the examiner
  • 4/5: movement possible against some resistance by the examiner
  • 5/5: normal muscle strength.

Partial paresis in the left lower limb (3/5 in the Lovett score) and slight paresis of the right lower limb (4/5 in the Lovett score) was present. Positive bilateral Babinski sign was still present. The girl was ambulating with the assistance of the walker.

Deep tendon reflexes

  • Ensure that the patient is comfortable and relaxed and that you can see the muscle being tested.
  • Use a tendon hammer to strike the tendon of the muscle and look for muscle contraction.
  • Compare both sides.
  • Reflexes can be hyperactive (+++), normal (++), sluggish (+) or absent (-). ± is used when the reflex is only present on reinforcement (see below).

In the upper limbs

  • Test the biceps jerk (C5, C6) – with their arm relaxed, hold the patient’s elbow between your thumb and remaining fingers, your thumb being anterior and directly over the biceps tendon. Ideally, the elbow should be held at 90°. Elicit the reflex by tapping on your thumb.
  • Test the triceps jerk (C6, C7) – with their arm relaxed, hold the patient’s arm across their lower chest/upper abdomen with one of your hands. Elicit the reflex by tapping over the triceps tendon just above and behind their elbow.
  • Test the supinator jerk (C5, C6) – ask the patient to relax their arm across their abdomen. Elicit the reflex by tapping over the supinator tendon just above the wrist.
  • Test the finger jerk – with their hand relaxed, place the tips of your index and middle fingers across the palmar surface of the patient’s proximal phalanges. Tap your fingers lightly with the tendon hammer. There should be slight flexion of the patient’s fingers. If there is hyperreflexia, this flexion is exaggerated.
  • Test the Hoffmann’s reflex – rest the distal interphalangeal joint of the patient’s middle finger on the side of your right index finger. Use the tip of your right thumb to flick down on the patient’s middle fingertip. Watch for any movement of the patient’s thumb as their fingertip springs back up. Normally there is no movement; in hyperreflexia, thumb flexion can be seen.
  • If a reflex is difficult to elicit, try ‘reinforcement’ (the Jendrassik maneuver). Ask the patient to clench their teeth or squeeze their knees together while you try to elicit the reflexes again.

Interpretation

  • Upper motor neuron lesions usually produce hyperreflexia.
  • Lower motor neuron lesions usually produce a diminished or absent response.
  • Isolated loss of a reflex can point to a radiculopathy affecting that segment – eg, loss of biceps jerk if there is a C5-C6 disc prolapse.

Examination of co-ordination

  • The cerebellum helps in the coordination of voluntary, automatic and reflex movement. Tests of cerebellar function, however, are only valid if power and tone are normal, and that failure to perform them may also be related to power and tone abnormalities in the upper limb rather than a cerebellar problem. These include

The finger-nose test

  • The patient should keep their eyes open.
  • Hold one of your fingertips up in front of and a short distance (about 30-40 cm) from the patient.
  • Ask the patient to touch the tip of their nose and then to touch your fingertip alternately and repeatedly. You can continuously change your fingertip position to make the test more difficult.
  • You can then test for sensory ataxia by asking the patient to close their eyes and to touch the tip of their nose using their outstretched finger.
  • Repeat these tests on the other side.
  • Look for intention tremor and past-pointing as the patient touches the examiner’s fingertip, which can indicate disease of the cerebellar hemispheres.

Rapid alternating movement

  • The patient needs to have one palm facing upwards.
  • They need to touch this palm with the palmar and then dorsal sides of the fingertips of the other hand as quickly as possible. Note that they must lift the second hand between each movement and touch the same point on the other palm without rolling the hand.
  • Test both sides. It is normal for the dominant hand to be a little faster at this test.
  • Look for dysdiadochokinesis. This is in coordination or slow movement when trying to perform this test.
DERMATOME DISTRIBUTION (1)
DERMATOME DISTRIBUTION (2)

A note about sensation in the hand

  • The hand may require more intensive testing. It may be useful to return to it after testing the rest of the arm.
  • Test sensation on both the palmar and the dorsal aspects.
  • Be aware of the distribution of the median, ulnar and radial nerves:[1]
    • The radial nerve supplies sensation to the skin on most of the dorsum of the hand.
    • The ulnar nerve supplies sensation to the palmar aspect of the little finger and the palmar aspect of the medial half of the ring finger. It also supplies the distal half of the dorsal aspect of these fingers.
    • The median nerve supplies sensation to the palmar aspect of the thumb, index and middle fingers and the lateral half of the ring finger. It also supplies the distal half of the dorsal aspect of these fingers.
Image result for Brown-Séquard syndrome
www.rxharun.com

Interpreting the findings

The site of any lesion can be determined by looking at the pattern of any dysfunction found. The dermatomal (segmental) and peripheral nerve innervation is labeled in the diagrams above.

  • All of the sensory modalities can be affected in peripheral neuropathies and nerve injuries, cervical radiculopathy, and spinal injuries.
  • If an individual nerve or sensory root is affected, all sensory modalities can be reduced.
  • If there is a spinal cord lesion, there may not be equal diminution across all of the sensory modalities: light touch, vibration, and joint position sense may remain intact while sharp touch and temperature are lost. This is because the lateral spinothalamic pathways may be damaged while the dorsal columns remain intact. Cervical syringomyelia is an example where this may happen.
  • Problems with joint position sense or vibration usually occur distally first.
  • Vibration sense can be lost before joint position sense in peripheral neuropathy or myelopathy affecting the dorsal columns.
  • Parietal lobe lesions can also cause impairment of two-point discrimination.

Ask about the Symptoms

  • What are they?
  • Which part of the body do they affect? Are they localized or more widespread?
  • When did they start?
  • How long do they last for?
  • Were they sudden, rapid or gradual in onset? Is there a history of trauma?
  • Are the symptoms static or deteriorating, or are there exacerbations and remissions? For example, worsening of symptoms with hot environments – eg, sauna, hot bath or hot weather in demyelinating disorders (called Uhthoff’s sign).
  • Does anything trigger the symptoms – eg, exercise, sleep, posture or external stimuli such as light or smell?

Ask about any associated symptoms (other features of neurological disease)

  • A headache.
  • Numbness, pins and needles, cold or warmth.
  • Weakness, unsteadiness, stiffness or clumsiness.
  • Nausea or vomiting.
  • Visual disturbance.
  • Altered consciousness.
  • Psychological changes – eg, agitation, tearfulness, depression or elation, sleep disturbance.
  • For children, ask about performance at school.

Try to understand how the symptoms may affect the patient’s life – ask about activities of daily living. The distal parts of the limbs tend to be affected in polyneuropathy, the legs usually being involved before the arms. A ‘glove and stocking’ effect is produced.

  • Note any problem with articulation (dysarthria). Here comprehension is retained and speech construction is normal. There is usually weakness or incoordination of the orolingual muscles. Ask the patient to say ‘West Register Street’ if you are uncertain.
  • Note any problem with phonation (dysphonia). This is usually due to laryngeal problems which can cause voice hoarseness. There may be reduced speech volume.
    • Look at the patient’s gait as they enter the room.
    • Note if there evidence of, for example, hemiparesis, foot drop, ataxic gait, a typical Parkinsonian gait.
    • See separate Abnormal Gait and Gait Abnormalities in Children articles. Note any problem with language function (dysphasia). This is due to a lesion in the language areas of the dominant hemisphere.
      Chiropractic manipulation – Rare, but reported

There is more than one way of performing a neurological examination and a clinician should develop their own technique. Poor technique will fail to elicit signs or will produce false results.

Involuntary movements

Establish whether there is evidence of involuntary movements – for example, tremor, tics, chorea, hemiballismus, or orofacial dyskinesias.

Specific emphasis should be placed on the following:

Past medical history

Some neurological problems can present years after a causative event.

  • Enquire about other medical problems, past and present. These may give clues to the diagnosis. For example:
    • A person in atrial fibrillation may be producing multiple tiny emboli.
    • There may be vascular problems or recurrent miscarriage to suggest antiphospholipid syndrome.
    • There may be diabetes mellitus.
  • Ask about pregnancy, delivery, and neonatal health.
  • Ask about any infections, convulsions or injuries in infancy, childhood or adult life. Particularly ask about the head or spinal injury, meningitis or encephalitis.

Systematic Inquiry

The systematic inquiry is very important here. For example

  • Loss of weight and appetite may suggest malignancy and this may be a paraneoplastic syndrome.
  • The gain in weight may have precipitated diabetes mellitus.
  • Polyuria may suggest diabetes mellitus. The difficulty with micturition or constipation may be part of the neurological problem but was not volunteered in the general history. In men, enquire about erectile dysfunction.

Social history

  • Note smoking and drinking habits. Alcohol is a significant neurotoxin, both centrally and peripherally.
  • Ask about drugs, including prescribed, over-the-counter and illicit (such as cocaine usage that can be linked to cardiovascular problems). This includes complementary and alternative medicines.
  • Ask about occupation and what it involves. There may be exposed to toxins. Is repetitive strain injury likely? Is there prolonged visual work which may predispose tension-type headache migraine? The job may involve driving but the patient has admitted to convulsions. He/she may work at heights or in a dangerous environment.
  • Ask about marital status. Has there been recent bereavement or divorce which may have affected symptoms?
  • Ask about sexual orientation and consider the likelihood of sexually transmitted infection – eg, syphilis, HIV.

Family history

Consider if there may be a genetic basis or predisposition. For example:

  • A cousin with Duchenne muscular dystrophy or Becker’s muscular dystrophy would be very important for a boy who cannot run like his peers.
  • Huntington’s chorea is unusual in that it is a familial disease that does not present until well into adult life.
  • A family history of, for example, type 2 diabetes mellitus, cerebral aneurysm, neuropathies, epilepsy, migraine or vascular disease may be important.

Examination of speech

  • Look for spontaneous speech, fluency and use of appropriate words during conversation.
  • Ask the patient to name objects.
  • Ask the patient to carry out some commands to assess their comprehension.
  • Ask the patient to read aloud. This can show evidence of any dyslexia.
  • Ask the patient to repeat a simple sentence. Inability to do this suggests a conduction dysphasia.
  • Look at the patient’s handwriting. There may be problems with the form, grammar or syntax, which may suggest a more global language problem and not just a speech disorder.

Examination of the Neck

Examine the neck movements

  • Is there evidence of degenerative disease which may be producing radicular symptoms in the upper limbs? Examine flexion, extension, and rotation.
  • Look for Lhermitte’s sign: neck flexion causes an electric shock-like feeling on the limbs. It is due to disease in cervical spinal cord sensory tracts (seen in, for example, multiple sclerosis, syringomyelia, tumors).
  • Is there any neck stiffness? This can be a sign of meningeal irritation. The chin can normally touch the chest when the neck is flexed but this is not possible if neck stiffness is present. This may be a sign of meningitis or subarachnoid hemorrhage.

Palpate the supraclavicular fossae

  • Look for enlarged lymph nodes or cervical ribs.

Listen for any bruits

  • Listen at the carotid bifurcation at the angle of the jaw for carotid bruits.
  • Listen over the supraclavicular fossa for vertebral or subclavian bruits.
  • A common carotid bruit may be heard by listening between these two sites.
  • Listen with the bell of the stethoscope over a closed eyelid for bruits due to cerebral arteriovenous malformations.
  • Listen for cardiac murmurs to ensure that any bruit heard is not just due to the transmission of these.
  • Note that just because a bruit is not heard, it does not mean that there is no significant stenosis present.
  • Patients should have a full neurological examination and systemic examination. Investigations for any possible underlying cause may be required.
  • Nerve conduction studies – eg, to assess whether the lesion is axonal or demyelinating, or whether any entrapment is present.
  • Electromyography.
  • Ultrasound may be useful in some situations – eg, compression neuropathy.
  • MRI scan may help to evaluate brachial and lumbosacral neuropathies and may have more use in the future.
  • A nerve biopsy may be required.

Brown Sequard Syndrome Treatment

In treating the persons with Brown Sequard Syndrome, the treatments are aimed at the pathological cause of the syndrome.

Transfusion of blood

If, for instance, the etiological factor is because of a gunshot wound, the treatment is needed to be given instantly for this is an emergency situation because major bleeding and organ damage may occur, leading to a possible death of the person.

Immobilization

Yet, if the person has the syndrome primarily because there is a fracture of the spine which is needed to be identified as soon as possible to prevent further more complication and needs to be appropriately treated. Whenever the person is experiencing either injury of the cervical region or in the spinal cord, there is a need to immobilize the person.

Medication

Steroids

The use of high-dose steroids in the presence of spinal injury used to be the standard of care and was included as part of many SCI guidelines. In the past several years, this practice has been called into question and many studies have addressed this controversy. Although currently controversy still exists surrounding the use of steroids, the practice has been removed from guidelines and is no longer considered the standard of care.

The purpose of steroids in spinal cord injury was originally thought to be of benefit in three distinct ways. Steroids were thought to improve blood flow to the injured area of the spinal cord, assist in limiting the inflammatory response to injury, and reduce vasogenic shock and edema.

Through corticosteroids, the drug will reduce the inflammation found in persons with Brown Sequard syndrome.

Other treatment may be done:

  • Occupational therapy
  • Recreational therapy
  • Physical therapy
  •  Maintaining strength in neurologically intact muscles
  • Maintaining range of motion in joints
  • Preventing skin break down by proper positioning and weight shifting
  • Improving respiratory function by positioning and breathing exercise
  • Providing emotional and education support
  • Surgical therapy

Brown Sequard Syndrome Complication

Both the late and early complications that are associated with this kind of syndrome include the following:

    • Depression
    • Infection
    • Pulmonary embolism
    • Hypotension
    • Disk herniation
    • Vertebral artery dissection
    • Fracture
    • Spinal cord spasm
    • Fibromyalgia
    • Pressure ulcers
    • Bowel impaction


References

Brown-Séquard syndrome

Print Friendly, PDF & Email

Sharing to Spread to the World

61 thoughts on “Brown-Séquard Syndrome; Cause, Symptom, Treatment”

Leave a Reply

Your email address will not be published.