Brown-Sequard's Syndrome Flashcards

1
Q

What is brown-sequard syndrome?

A

Brown-Séquard’s syndrome results from a lesion in one (lateral) half of the spinal cord (for example, hemisection or lateral injury of the cord). It often occurs in the cervical cord region.

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2
Q

How does BS syndrome present?

A

The syndrome is rare and comprises ipsilateral hemiplegia with contralateral pain and temperature sensation deficits (because of the crossing of the fibres of the spinothalamic tract).

There is a total ipsilateral loss of position, light touch and vibration sensation at the level of the lesion.

There is contralateral loss of pain and temperature beginning a few segments below the lesion (because the spinothalamic tracts enter the cord and travel ipsilaterally for a few segments before decussating). No plantar response on this side because of loss of pain sensation.

There is ipsilateral spastic paraparesis with loss of vibration and joint-position sense (destruction of ipsilateral dorsal column fibres) below the lesion. Reflexes are brisk with upgoing plantar reflex.

There may be an ipsilateral Horner’s syndrome if the sympathetic fibres are damaged (in the neck).

There are also sphincter disturbances.

Incomplete forms of the syndrome commonly occur, usually caused by vascular impairment secondary to compression of the cord, with sparing of the dorsal columns (separate vascular supply); or inflammatory lesions (for example, multiple sclerosis).

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3
Q

What is the pathophysiology of BS syndrome?

A

The pure Brown-Séquard’s syndrome reflecting hemisection of the cord is rarely seen. However, a clinical picture with some of the features of the syndrome is more common.

The hemisection syndrome may also occur with additional symptoms and signs.

Interruption of the lateral corticospinal tracts, the lateral spinothalamic tract, and occasionally the posterior columns clinically causes a spastic weak leg with brisk reflexes and a strong leg with loss of pain and temperature sensation.

Spasticity and hyperactive reflexes may not be present with an acute lesion.

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4
Q

What is the aetiology of BS syndrome?

A

The causes of this syndrome are:

  • Most commonly, trauma (penetrating or blunt).
  • Neoplasia (spinal cord tumour - either metastatic or primary).
  • Multiple sclerosis.
  • Degenerative (such as herniation of discs and cervical spondylosis).
  • Cysts and cystic diseases.
  • Idiopathic spinal cord herniation. (Spinal cord herniation can also occur after trauma.)

Vascular causes:

  • Haemorrhage (including spinal subdural/epidural and haematomyelia).
  • Ischaemia.

Infectious causes: e.g., meningitis, empyema, herpes zoster virus, herpes simplex virus, tuberculosis, syphilis.

Other causes: include gnathostomiasis (helminthic parasitic disease), and tropical spastic paraplegia (HTLV-1).

Rollercoaster riding and chiropractic manipulation may be a contributing factor if there is a predisposition (such as a cyst).

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5
Q

What are the differentials of BS syndrome?

A

Diagnosis is made on patient assessment.

Most cases will be caused by trauma.

When there is no hx of trauma, it is important to consider:

  • MS
  • Spinal cord injury and compression
  • Stroke
  • Spinal tumours
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6
Q

What are the investigations for BS syndrome?

A

Spinal plain radiographs (for bony injury in penetrating or blunt trauma).

MRI scanning can help to define the extent of spinal cord injury. It is particularly helpful when evaluating non-traumatic causes.

MRI may be needed in traumatic cases when there is neurological deterioration.

CT myelography (useful if MRI is contra-indicated).

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7
Q

What is the management of BS syndrome?

A

Initially, a thorough evaluation, including neurological examination, is performed to establish the level of injury.

Careful cervical spine/dorsal spine immobilisation is necessary.

No movement of the neck should be permitted.

It is important to identify cases (such as spinal cord herniation) where surgical intervention can improve prognosis

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8
Q

What are the complications of BS syndrome?

A

Early and late complications may occur.

These include:

  • Hypotension (spinal shock)
  • PE
  • Infection (lungs, urine)
  • Depression
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9
Q

What is trigeminal neuralgia?

A

Trigeminal neuralgia (TN) can be described as a chronic, debilitating condition resulting in intense and extreme episodes of pain in the face.

The episodes are sporadic and sudden and often like ‘electric shocks’, lasting from a few seconds to several minutes.

TN results from a neuropathic disorder of the Vth cranial nerve (trigeminal nerve).

The trigeminal nerve senses mixed modalities including:
o Sensation.
o Nociception.
o Thermoception.
o Motor supply to the muscles of mastication.

Most commonly, the maxillary and/or mandibular branch are involved.

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10
Q

What is the cause of TN?

A

In nearly all cases, TN is thought to be caused by compression of the trigeminal nerve by a loop of artery or vein; another 5%-10% of cases are attributed to tumours, multiple sclerosis, abnormalities of the skull base, or arteriovenous malformations.

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11
Q

What is the presentation of TN?

A

TN is a sudden, unilateral, brief, stabbing, recurrent pain in the distribution of one or more branches of the Vth cranial nerve.

Pain occurs in paroxysms which last from a few seconds to two minutes. The frequency of the paroxysms ranges from a few to hundreds of attacks a day.

Periods of remission can last for months to years but tend to shorten over time.

There may be preceding symptoms – e.g., tingling or numbness.

Patients may have certain triggers that set the pain paroxysm off.

This is followed by sharp, severe, shock-like pains.

These pains are usually on one side in the cheek or face, but pain can involve the eyes, lips, nose and scalp.

Episodes are intermittent but can last days, weeks or months on end and then not return for months or even years.

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12
Q

What are the triggers of TN?

A
Vibration.
Skin contact - eg, shaving, washing.
Brushing teeth.
Oral intake.
Exposure to wind.
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13
Q

What is atypical TN?

A

Relentless underlying pain like a migraine associated with superimposed stabbing pains.

There may also be an intense burning sensation. This condition is particularly difficult to treat.

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14
Q

What is the diagnostic criteria for TN?

A

Site: pain is unilateral in the distribution of the trigeminal nerve, bilateral in only 3% of patients, and rarely is the pain active on both sides at the same time.

Periodicity: episodic and sudden onset of pain, lasting a few seconds to minutes and stopping suddenly, with many attacks a day. There is a refractory period between each attack. Pain might then go into remission for weeks or months; pain-free intervals gradually shorten between episodes.

Character: electric shock-like, sharp, shooting.

Severity: very severe attacks, but attacks can get milder when patients are given drug treatment.

Factors affecting pain: can be provoked by light touch to the face, eating, cold winds, or vibrations.

Associated factors: rarely associated with history of other chronic pain or migraine. Some forms have more continued aching background pain after main attack. Rarely associated with autonomic features.

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15
Q

What are the red flags of TN?

A

Sensory changes, deafness or other ear problems.

Difficulty achieving pain control, poor response to carbamazepine.

History of any skin lesions or oral lesions that could lead to perineural spread.

Ophthalmic division only or bilateral as suggestive of benign or malignant lesions or multiple sclerosis.

Age of onset under 40 years.

Optic neuritis.

Family history of multiple sclerosis.

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16
Q

What are the differentials of TN?

A
Dental pathology 
Temporomandibular joint dysfunction 
Migraine 
GCA- TN rarely affects the forehead alone. 
Cluster headaches 
MS 
Overlying aneurysm of a blood vessel 
Tumour in the posterior fossa- meningiomas
Postherpetic neuralgia after shingles
17
Q

What are the investigations of TN?

A

MRI brain to rule other potential causes of pain such as :
Sinusitis.
Extracranial masses along the course of the trigeminal nerve.
Pathological enhancement of the trigeminal nerve that could indicate perineural spread of malignancy.
Cavernous sinus masses.
Demyelination plaques that might indicate multiple sclerosis.
Intrinsic brain lesions in the thalamus or trigeminal brain stem pathways such as lacunar infarctions.
Cerebellopontine angle mass lesions such as tumour, epidermoid, dermoid, or arachnoid cyst, aneurysm, or arteriovenous malformation.

18
Q

What is the management of TN

A

No definitive cure
NICE recommends:
o Offer carbamazepine as initial treatment for TN.
o If initial treatment with carbamazepine is not effective, is not tolerated or is contra-indicated, consider seeking expert advice from a specialist and consider early referral to a specialist pain service or a condition-specific service.

Patients need to be made aware that the condition is not life-threatening.

There is a need, however, also to express empathy towards severity of the condition.

Education as to the causes and potential therapies.

Reassurance and support groups.

Consider referring the person to a specialist pain service or a relevant clinical speciality (for example, neurology, diabetology, or oncology services)

Gabapentin combined with regular ropivacaine injections into trigger sites has been shown to improve pain control and quality of life, and pregabalin was found to be effective at one-year follow-up.

Botulinum toxin type A (BTX-A) in TN produces a response in approximately 70%-100% of patients.

Surgery involves either relieving pressure on the trigeminal nerve or damaging it to prevent any pain transmission.

19
Q

When should you refer a patient with TN?

A

They have severe pain.

Their pain significantly limits their participation in daily activities (including self-care, general tasks and demands, interpersonal interactions and relationships, mobility, and sleeping).

Atypical clinical features (for example, burning pain between paroxysms, loss of sensation, or any abnormal neurological signs) are present.

20
Q

What are the types of surgery for TN?

A

Microvascular decompression

Rhizotomy

21
Q

What is microvascular decompression?

A
  • Microvascular decompression (MVD) aims to decompress the trigeminal nerve, and deals with the cause of TN in the majority of cases not caused by other lesional causes.
  • Blood vessels are compressing the trigeminal nerve, and lifting these blood vessels away reduces the pressure. This requires a general anaesthetic.
    -The approach is behind the ear into the posterior fossa on the affected side. Patients are usually assessed by MRI beforehand to look for the presence of compression.
22
Q

What is rhizotomy?

A

The aim of rhizotomy is to damage the trigeminal nerve. This is an alternative to the more invasive decompression. These methods include:

  • Percutaneous glycerol rhizotomy (under a local anaesthetic).
  • Percutaneous balloon compression rhizotomy (under a general anaesthetic).
  • Radiofrequency rhizotomy (performed under sedation).
23
Q

What is the complication of TN?

A

The pain of TN can be so intense that it can lead to a poor quality of life due to mental and physical incapacity. Patients may require psychosocial input – e.g., counselling.