Spinal Cord Compression

Spinal Cord Compression

Spinal Cord Compression

Spinal cord compression (SCC) results from processes that compress or displace arterial, venous, and cerebrospinal fluid spaces, as well as the cord itself.

This can occur as a result of extrinsic causes and lesions, or intrinsic aetiologies of the cord substance. Examples include trauma or tumor affecting the cord substance, and lesions that compromise cord function emanating from surrounding elements or vascular sources. 

The presenting symptoms are a result of spinal cord injury (SCI) or root dysfunction and include paresis, sensory changes or loss of sensation, sphincter dysfunction (urinary or anal), and erectile problems.

Causes of spinal cord compression

Trauma (including car accidents, falls and sports injuries):

    • There is usually either vertebral fracture (most common in cervical vertebrae) or facet joint dislocation.
    • Complete transection of the spinal cord can occur.
    • Hemisection of the spinal cord can occur and is known as Brown-Séquard’s syndrome. It is usually caused by a penetrating trauma.

Tumours, both benign or malignant:

    • These can include bone tumours, primary or metastatic tumours, lymphomas, multiple myeloma and neurofibromata.
    • Acute myelopathy in patients with cancer can also be caused by irradiation, paraneoplastic necrotising myelitis, ruptured intervertebral disc and meningeal carcinomatosis with spinal cord involvement.

A prolapsed intervertebral disc:

  • L4-L5 and L5-S1 are the most common levels for disc prolapse. Large disc herniations can cause cauda equina syndrome. 
    • Cervical disc herniation can also occur.

An epidural or subdural haematoma:

    • There may be a history of trauma, a recent spinal procedure and/or the patient may be on anticoagulant therapy.

Inflammatory disease, especially rheumatoid arthritis:

    • In rheumatoid arthritis there is often considerable weakness of the ligament that holds the odontoid peg. If this ruptures, the atlas can slip forward on the axis and compress the high cervical spine.

Infections:

    • Spinal infections can be acute or chronic.
    • Acute infections are usually bacterial; chronic infections are usually due to tuberculosis or fungal infection.
    • Vertebral osteomyelitis, discitis or haematogenous spread of infection can lead to an epidural abscess.

Cervical spondylitic myelopathy:

    • The ageing process can lead to narrowing of the spinal canal due to osteophytes, herniated discs and ligamentum flavum hypertrophy.
    • In advanced stages, it can cause spinal cord compression.

Spinal manipulation:

    • Damage to the spinal cord may be a very rare complication of chiropractic or osteopathic manipulation of the neck.

Clinical Presentation

  1. Neurological symptoms: gait disturbance, clumsy or weak hands, or loss of sexual, bladder, or bowel function.
  2. Neurological signs:
    • Lhermitte’s sign: flexion of the neck causes an electric shock-type sensation that radiates down the spine and into the limbs.
    • Upper motor neurone signs in the lower limbs (Babinski’s sign: up-going plantar reflex, hyperreflexia, clonus, spasticity).
    • Lower motor neurone signs in the upper limbs (atrophy, hyporeflexia).
    • Sensory changes are variable, with loss of vibration and joint position sense more evident in the hands than in the feet.
  3. Motor, sensory and autonomic dysfunction can occur. The latter can lead to neurogenic shock, paralytic ileus, aspiration, urinary retention, priapism and loss of thermoregulation. Clinical features depend upon the extent and rate of development of cord compression.
  4. Motor symptoms can include ready fatigue and disturbance of gait.
  5. Cervical spine lesions can produce quadriplegia. Injury above the level of C3, C4, C5 (the segmental level of the phrenic nerve) cause paralysis of the diaphragm and artificial ventilation is required.
  6. Thoracic spine lesions produce paraplegia.
  7. Lumbar spine lesions can affect L4, L5 and sacral nerve roots.
  8. Sensory symptoms can include sensory loss and paraesthesia. Light touch, proprioception and joint position sense are reduced.
  9. There can be root pain in the legs.
  10. Tendon reflexes are typically:
    • Increased below the level of injury and/or compression.
    • Absent at the level of injury and/or compression.
    • Normal above the level of injury and/or compression.
  11. Sphincter disturbances – late features of cervical and thoracic cord and/or compression.
  12. There may be loss of autonomic activity with lack of sweating below the level, loss of thermoregulation and drop in peripheral resistance causing hypotension.

Investigations

  • Haemoglobin and haematocrit levels should be measured initially and monitored serially to monitor blood loss.
  • Renal function and electrolytes: dehydration.
  • MRI scan of the whole spine.
  • Further investigations will depend on the underlying cause for cord compression.

Management

  1. Nurse the patient flat with the spine in neutral alignment (eg, using logrolling or turning beds) until spinal stability and neurological stability are ensured.
  2. Give a course of dexamethasone unless contra-indicated until a definitive treatment plan is made.
  3. Manage postural hypotension with positioning and devices to improve venous return; avoid over hydration.
  4. Insert a catheter to manage bladder dysfunction.
  5. Use breathing exercises, assisted coughing, and suctioning to clear airway secretions.
  6. Offer and provide psychological and spiritual support as needed (including after discharge).
  7. Analgesia, palliative radiotherapy, spinal orthoses, vertebroplasty or kyphoplasty, or spinal stabilization surgery may be required for pain control.
  8. Bisphosphonates should be offered to all patients with vertebral involvement from myeloma and breast cancer and to patients with prostate cancer in whom conventional analgesia is inadequate.
  9. Specialized pain control procedures may be needed for intractable pain (eg, epidural analgesia).
  10. If definitive treatment of the cord compression is appropriate, it should be started before patients lose the ability to walk or before other neurological deterioration occurs, and ideally within 24 hours.
  11. Definitive treatment may be using surgery (eg, laminectomy, posterior decompression ± internal fixation) or using radiotherapy.
  12. Discharge should be fully planned and community-based rehabilitation and support should be available when the patient returns home. This includes support and any necessary training of carers and families.

Cancer Screening.

  1. The following symptoms suggest possible spinal metastases in those with cancer:
    • Pain in the thoracic or cervical spine.
    • Severe unremitting or progressive lumbar spinal pain.
    • Spinal pain aggravated by straining (eg, coughing, sneezing, passing stool).
    • Nocturnal spinal pain preventing sleep.
    • Localised spinal tenderness.
  2. The following symptoms suggest metastatic spinal cord compression in patients with cancer and pain suggestive of spinal metastases:
    • Radicular pain.
    • Limb weakness.
    • Difficulty in walking.
    • Sensory loss, or bladder or bowel dysfunction.
    • Neurological signs of spinal cord or cauda equina compression.
  3. MRI of the whole spine (not plain X-rays) should be carried out so that definitive treatment can be planned. This should be:
    • Within one week if clinical features suggest spinal metastases.
    • Within 24 hours if clinical features suggest spinal cord compression.
    • Sooner (including out of hours) if emergency treatment is needed.

Complications

Complications will depend on the site of compression and the severity of associated neurological dysfunction. Complications may include:

  • Pressure sores: careful and frequent turning of the patient is essential.
  • Hypothermia.
  • Potential lung complications include aspiration, pneumonia, acute respiratory distress syndrome, atelectasis, ventilation-perfusion mismatch and decreased coughing with retention of secretions.
  • Depression associated with restriction of activities of daily living.

Prognosis

  • The spinal cord has very limited powers of regeneration.
  • Prognosis for neurological deficit depends on the magnitude of the spinal cord damage present at the onset.
  • As well as neurological dysfunction, the prognosis is also determined by the prevention and effective treatment of infections – eg, pneumonia, and urinary tract infections.
  • The prognosis will also depend on the underlying cause of cord compression.

General Paralysis of The Insane (GPI)

General paralysis of the insane (GPI) also known as General paresis, paralytic dementia, or syphilitic paresis is a severe neuropsychiatric disorder, classified as an organic mental disorder and is caused by late-stage syphilis and the chronic meningoencephalitis and cerebral atrophy that are associated with this late stage of the disease when left untreated.

Degenerative changes caused by GPI are associated primarily with the frontal and temporal lobar cortex. The disease affects approximately 7% of individuals infected with syphilis, and is far more common in third world countries where fewer options for timely treatment are available. It is more common among men.

Signs and symptoms

Symptoms of the disease first appear from 10 to 30 years after infection.

Early Signs and Symptoms

  • Neurasthenia (mechanical weakness of nerves) difficulties, such as
  • fatigue,
  • headaches,
  • insomnia,
  • dizziness, etc.

 Signs and Symptoms as the disease progresses;

  • mental deterioration and personality changes occur
  • Typical symptoms include loss of social inhibitions,
  • gradual impairment of judgment,
  • concentration and short-term memory impairment, 
  • euphoria – intense feeling of pleasure.
  • Mania – mental and behavioral disorder characterized by abnormally elevated arousal, affect, and energy level.
  • Depression – mental state of low mood and eversion to activity.
  • apathy – is a lack of feeling, emotion, interest or concern about something.
  • Subtle shivering,
  • minor defects in speech
  • Delusions – They can be grandiose, melancholic, or paranoid. These delusions include ideas of great wealth, immortality, thousands of lovers, unfathomable power, nihilism, self-guilt, self-blame, or bizarre hypochondriacal complaints.

Late Signs and Symptoms

  • Dysarthria – condition in which problems effectively occur with muscles that help produce speech, hence a sound disorder resulting from neurological injury of the motor speech system.
  • intention tremors – dyskinetic disorder
  • Hyperreflexia – overresponsive bodily reflexes
  • myoclonicjerks – involuntary, irregular twitching of muscles
  • confusion,
  • seizures and severe muscular deterioration.
  • Eventually, the paretic dies bedridden, cachectic(complex syndrome associated with underlying illness causing ongoing muscle loss that is not entirely reversed with nutritional supplements) and completely disoriented, frequently in a state of status epilepticus(single seizure lasting more than 5 min, or 2 or more seizures within a 5-minute period without a person returning to normal between them)

Diagnosis

  • Definitive diagnosis is based on the analysis of cerebrospinal fluid and tests for syphilis.
  • Physical Examination

Treatment

  • Using penicillin or other antibiotics to treat the infection.
  • Treatment will likely continue until the infection has completely cleared. Treating the infection will reduce new nerve damage. But it will not cure damage that has already occurred.
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