Microvascular Decompression is a surgical procedure used to treat trigeminal neuralgia, hemifacial spasm, and glossopharyngeal neuralgia caused by compression of cranial nerves by blood vessels. The procedure involves using a microscope to identify the compressing blood vessel and place a small piece of Teflon between the nerve and vessel to relieve compression. It provides long-term pain relief with few complications when performed by an experienced surgeon for patients who have not responded well to medications.
2. Introduction
The pathobiology of vascular compression of the trigeminal (V), facial (VII), glossopharyngeal
(IX), and vagus (X) nerves underlies a number of related neurologic disorders.
Dandy (1932) first described vascular compression of the trigeminal nerve in the posterior fossa
as a potential cause of trigeminal neuralgia, termed tic douloureux.
Gardner and Sava (1962) identified vascular compressive lesions of the facial nerve as the likely
underlying etiology of hemifacial spasm
Jannetta (1967) used the microscope to systematically study vascular compression of cranial
nerves, termed microvascular decompression (MVD).
3. Trigeminal Neuralgia
• Most common cranial nerve vascular compression syndrome.
• Female : Male = 2:1
• Peak onset 50-70yo
• Most common affected branches : V2 and/ V3
• Unilateral pain (1% patients bilateral)
4.
5. Clinical presentasion:
• Proxysmal, intense, intermittent pain
• Described as an intense stabbing or electrical shock-like sensation,
lasting seconds to minutes
• Triggered by light cutaneous stimuli
• Episodic free of pain between pain attacks
• Occasionally patients suffer from both trigeminal neuralgia and
hemifacial spam, known as tic convulsif.
Trigeminal Neuralgia
6. • Differential diagnosis
• Multiple sclerosis: can causes paroxysmal attacks of Trigeminal facial pain
• Isolated orbital pain syndromes (low onset, hours to days)
• Cluster headache (insidious onset, runny nose, ptosis or watery eye)
• Postherpetic neuralgia (constant pain with vesicles)
• Dental disease (site spesific)
• TMJ dysfunction
• Temporal arteritis (tenderness over STA)
• Posttraumatic neuralgia
Trigeminal Neuralgia
7. Imaging: High-resolution MRI of posterior fossa
• T1
• sequence: whole brain axial and sagittal (volumetric when possible)
• purpose: anatomical, brain screen
• T2
• sequence: axial, limited to posterior fossa (medulla to the upper pons) with thin slices (e.g. 3D
CISS and FIESTA)
• purpose: assess the N. trigeminal from their origin at the mid pons anteriorly, through
the prepontine cistern until the Meckel’s cave (trigeminal ganglion)
• the most common cause of trigeminal neuralgia is an enlarged looping artery (most commonly the superior
cerebellar artery) or vein pressing on the trigeminal nerve at the CPA , which is best depicted by this sequence
• FLAIR
• sequence: whole brain axial
• purpose: white matter signal abnormality such as in multiple sclerosis
• T1 C+ (Gd)
Trigeminal Neuralgia
8.
9. Medical management
• First-line medications: (blockade of voltage-sensitive sodium channels,
quelling hyperexcited neurons)
• Carbamazepine, started dose 2x100mg, increased by 100mg/day until pain control is
achieved or toxicity develops. Typical maintenance dose 300-800mg/day
• Oxcarbazepine, started dose 2x150mg. Increased by 300mg every 3 days until pain
relief. Maintenance dose 2 x 300—600mg
• Second-line medications:
• Baclofen, 10-80mg/day (GABAB receptors agonist, depresses excitatory neuroal
activity)
• Lamotrigine, initial dose 25mg/day, titrated up to 200-400mg/day
• Other: phenytoin, clonazepam, gabapentin, pregabalin, topiramate, leviracetam,
valproate.
Trigeminal Neuralgia
18. Postoperative care
• Observe any neurologic sign of posterior fossa pathology, due to
either cerebellar swelling or hematoma
• Oral intake
• Initiate DVT prophylaxis on the 1st postop day
• Surgical dressing is removed on 2nd postop day
• Headache postop controlled with narcotic analgetic
• Discharge by second or third postop day
Trigeminal Neuralgia
22. Hemifacial Spasm
Clinical features
• Most frequently on female
• Mean age of onset of 45 yo
• Repetitive, painless paroxysmal twitching of facial muscles (starts with
the orbicularis oculi and periorbital muscles and then slowly progresses
to middle and lower facial musculature).
• Significantly worsens during period of stress or anxiety psychogenic
or emotional problems
23. EMF findings
• 5-20 rhythmic burst discharge/
second, can lead to 150-250
bursts / second
Hemifacial Spasm
26. Medical management
• Botulinum toxin injection (release acetylcholine from presynaptic
nerve terminal).
• Carbamazepine, gabapentin, clonazepam, and baclofen
Hemifacial Spasm
27. Surgical indications
• Good health
• Younger than 75yo
Surgical options
• MVD (best choice)
• Neurotomy
• Distal nerve avulsion
• Facial nerve sectioning (with or without anastomosis to hypoglossal or
accessory nerve)
Hemifacial Spasm
28. Perioperative considerations
• Lateral or park bench position with modification rotating head 10-20
degress toward to floor (improve exposure of the lower cranial
nerves)
• Intraoperative monitoring of N.VII (EMG) dan N.VIII (Brain stem
auditory evoked respons) is recomended.
Hemifacial Spasm
34. Glossopharyngeal Neuralgia
• Less common than TN, incidence 0,2-0,7/100.000/people/year
• female more frequently (2:1), more common in the left side
• Symptom onset most common observed in fifth decade
• Most idiopathic GN (severe demyelination and degeneration of N. IX
and X)
• Secondary GN occure due to compression by vascular, tumor CPA,
calcified stylohyoid, MS, pagets disease, etc
35. Diagnosis:
• Confirmed with topical cocaine (10%) in trigger zone relief from
painful 1-2 hours after stimulation
Imaging:
• High-resolution MRI of the posterior fossa
Medical management: carbamazepien, etc.
Glossopharyngeal Neuralgia
