Teflon for microvascular decompression

Microvascular decompression (MVD) for neurovascular compression syndromes, such as trigeminal neuralgia and hemifacial spasm, has been traditionally described as an interposing technique using Teflon.

Teflon™ and Ivalon® are two materials used in MVD for TN. It is an effective treatment with long-term symptom relief and recurrence rates of 1-5% each year. Ivalon® has been used less than Teflon™ though is associated with similar success rates and similar complication rates ¹⁾.

Synthetic materials, such as Teflon or Ivalon sponges have also been associated with a direct subsequent neurovascular compression by the same vessel because of a slipped prosthesis ²⁾.

Compression of the trigeminal root entry zone, caused by the prosthesis itself or by severe adhesions, has been reported by several authors ^{3) 4)} , and even indirect vascular compression caused by fairly hard implants like Ivalon has been reported ^{5) 6)}.

Two patients with a history of microvascular decompression (MVD) for hemifacial spasm who presented with Teflon granulomas (TG) mimicking cerebellopontine angle (CPA) tumors and to perform a systematic review of the English-language literature. STUDY DESIGN: Case series at a single tertiary academic referral center and systematic review. METHODS: Retrospective chart review with analysis of clinical, radiological, and histopathological findings. Systematic review using PubMed, Embase, MEDLINE, and Web of Science databases. RESULTS: Two patients with large skull base TGs mimicking CPA tumors clinically and radiographically were managed at the authors' institution. The first presented 4 years after MVD with asymmetrical sensorineural hearing loss, multiple progressive cranial neuropathies, and brainstem edema due to a growing TG. Reoperation with resection of the granuloma confirmed a foreign-body reaction consisting of multinucleated giant cells containing intracytoplasmic Teflon particles. The second patient presented 11 years after MVD with asymmetrical sensorineural hearing loss and recurrent hemifacial spasm. No growth was noted over 2 years, and the patient has been managed expectantly. Only one prior case of TG after MVD for hemifacial spasm has been reported in the English literature. CONCLUSIONS: TG is a rare complication of MVD for hemifacial spasm. The diagnosis should be suspected in patients presenting with a new-onset enhancing mass of the CPA after MVD, even when performed decades earlier. A thorough clinical and surgical history is critical toward establishing an accurate diagnosis to guide management and prevent unnecessary morbidity. Surgical intervention is not required unless progressive neurologic complications ensue ⁷⁾.

Takeda et al. report the successful treatment of a patient with hemifacial spasm due to a tortuous vertebral artery that appeared to have developed to compensate for agenesis of the ipsilateral carotid artery. The 51-year-old man presented with a 1-year history of progressive left hemifacial spasm. His medical history was otherwise unremarkable except for untreated mild hypertension. Magnetic resonance angiography and bone window computed tomography demonstrated congenital agenesis of the left carotid artery and compression of the root exit zone of the left facial nerve by a tortuous left vertebral artery (VA). Microvascular decompression was performed via a left suboccipital craniotomy, and the offending vessel was identified using endoscopy. The vertebral artery was successfully transposed using polytetrafluoroethylene (PTFE) tape and a PTFE ball (Bard PTFE felt, Tempe, Arizona). This is the first report of a patient with hemifacial spasm caused by an ectatic VA associated with agenesis of the ipsilateral carotid artery ⁸⁾.