Question

Write an Essay describing in your own words the following conditions:

• Bell Palsy
• Gillian Barre's Syndrome
• Trigeminal Neuralgia

Answer 1

Bell's palsy:

• Bell's palsy is the inflammation of the facial nerve above the stylomastoid foramen.
• This leads to a lower motor neuron type of facial nerve paralysis.
• The cause of bell's palsy is thought to be due to :
  • Viral infection (herpes simplex, Ebstein Barr's virus, cytomegalovirus, HIV )
  • Bacterial infection (syphilis, Lyme's disease, mycoplasm)
  • Autoimmunity
  • Hereditary (4%)
  • Increase predisposition is seen in patients with hypertension and diabetes
• Onset and progression:
  • Onset - Acute
  • Progression - by 2 days maximum paralysis is seen
  • BY 5 days complete paralysis is establised
• Clinical manifestations:
  • On the face:
    • Deviation of the mouth towards the normal side
      • The facial nerve supplies the muscles of the face.
      • These are pulling muscles.
      • When there is unilateral paralysis of the facial nerve, there is a unilateral facial paralysis.
      • There is an uninhibited pull of the muscle of the normal side.
      • This causes loss of wrinkles on the face
      • There is dribbling of saliva from the angle of the mouth.
    • Difficulty eating
    • Reduced closure of the eye
  • Ears - Hyperacusis - Abnormally high sensitivity to a particular sound that is perceived as normal by other people. (due to involvement of the nerve supply to the stapedius muscle)
  • Disturbance in taste sensation: due to involvement of the chorda tympani nerve.
  • Bell's phenomenon
    • Normally as one closes one's eye, the eyeballs roll upwards and inwards.
    • This can be seen on the affected side due to incomplete closure of the eyelid.
• Diagnosis is clinical, however, CT or MRI brain should be done to rule out any intracranial cause of paralysis.
• Treatment - 80% if the case resolves spontaneously (2-12 weeks), 10% may have a disfigurement. Taste sensation recovers before motor function.
• Other treatment modalities:
  • Protection of the eye.
  • Steroids to reduce the inflammation (Prednisolone)
  • Antiviral - Acyclovir

Gillian Barre's syndrome:

• It is an inflammatory demyelinating neuropathy.
• Pathophysiology:
  • This an autoimmune disease characterized by the development of auto-antibody against gangliosides.
  • These antibodies bind to the gangliosides at the nodes of Ranvier in the myelinated neurons. On binding to the gangliosides, there is the activation of the complement system.
  • This leads to the disruption of sodium channels. This impairs the propagation of action potential.
  • This leads to flaccid paralysis.
  • There is also demyelination.
• Clinical features:
  • History of antecedent infection
    • Respiratory infection - mycoplasma, influenza infection,
    • Gastrointestinal infection - campylobacterium jejuni
  • Muscle weakness (progresses over days to weeks)
    • It starts from the lower limbs and progresses to the upper limbs.
    • Proximal muscles are involved more than the distal muscles.
    • Trunk, bulbar, and respiratory muscles are involved.
    • Cranial nerve involvement: III, VII, IX, XII
    • Loss of deep tendon reflexes
  • Sensory - Loss of proprioception and pain (before the onset of loss of pain sensation, there may be complaints of deep aching pain) temperature sensation.
  • Autonomic involvement - Cardiac arrhythmia, postural hypotension.
• Diagnosis -
  • Clinical (history of infection followed by ascending paralysis with areflexia and loss of position sense)
  • CSF - increase in the CSF protein levels but not associated with an increase in pleocytosis.
  • Electrodiagnostic study:
    • Reduction in the conduction velocity
    • Conduction block
    • Prolong distal latencies
• Treatment -
  • Immunotherapy as early as possible (not effective after 2 weeks)
    • IV immunoglobulins
    • Plasmapheresis
  • Physiotherapy
  • Ventilatory support in patients who develop respiratory failure.
  • Deep venous thrombosis prophylaxis

Trigeminal neuralgia:

• Sudden unilateral stabbing pain in the area supplied by the trigeminal nerve.
• Etiology of the trigeminal neuralgia:
  1. The exact mechanism is unclear.
  2. Compression of the nerve root
  3. Demyelinating disorders like:
     1. Multiple sclerosis
     2. Hereditary sensory-motor neuropathy
  4. Malignancies of the head and neck that infiltrate the trigeminal nerve.
  5. Malignancies:
     1. Schwannoma
     2. Tumors of the cerebellopontine angle
     3. Meningioma
     4. Epidermal cyst
  6. Lesion of the pons and medulla
• Clinical features :
  1. Triggers:
     1. Shaving
     2. Showering
     3. Brushing teeth
     4. Exposure to wind
  2. The pain is stabbing, exploding, crushing, and shock like pain.
  3. Area of distribution - (rarely affects the ophthalmic division of the trigeminal nerve) - Cheek, jaw, forehead, gums, and lips.
  4. There is remission and exacerbation of the disease.
• Diagnosis based on history and clinical presentation
• CT or MRI brain to rule of intracranial lesion
• Treatment -
  1. Pain relief -
     • Carbamazepine
     • Oxacarbazepin
     • Lamotrigine
     • Baclofen
  2. Surgical treatment
     • Microvascular decompression - this is to relieve the nerve from compression in the mastoid area
     • Percutaneous radiofrequency trigeminal gangliolysis
     • Percutaneous retrogasserian glycerol rhizotomy - ablation of the nerve in the trigeminal cistern