Hemifacial Spasms and Involuntary Facial Movements. Role of Magnetic Resonance in the Diagnostic Work-up

Abstract

Caution is required when dealing with patients presenting hemifacial spasm as the symptom is common to many disorders (tumours, herpes zoster, a frigore paralysis, neurovascular conflict…). Often no reasonable cause of the spasm is found, but treatment must be attempted because hemifacial spasm can be highly debilitating. We describe a case of hemifacial spasm, initially deemed idiopathic, in which MRI demonstrated neurovascular conflict as the cause. It is not always easy to find a clear MRI pattern, but if the scan identifies the tortuousness of the arteries in the vicinity of the VII nerve root exit, it is highly probable that this is the true cause of hemifacial spasm. Even when it is not possible to identify this pattern, neurovascular compression cannot be ruled out. The good results of microvascular decompression in patients without a typical MRI pattern suggest that MRI is specific, but not always sensitive. There is no consensus in the literature on the sensitivity of MRI in the detection of neurovascular compression and values vary widely. It is generally believed that experience and different performance of the MR systems strongly influence the diagnosis of neurovascular conflict.

Developmental Venous Anomaly Responsible for Hemifacial Spasm

“…The term DVA was coined by Lasjaunias and now is widely used as a synonym for venous angioma, cerebral venous malformation or cerebral venous medullary malformation 6 . DVAs are congenital benign anatomic variations with angiogenically mature venous walls that lack arterial or capillary elements: it is hypothesized that they result from a focal arrest of venous development and retention of primitive medullary veins that drain into a single enlarged transcortical or subependymal collector vein which plays a compensatory role in relation to the absence of a normal cortical venous network 16 . These venous channels coalesce into a normal venous outflow tract and a focal stenosis may occasionally be noted as it enters the adjacent dural sinus predisposing to venous hypertension or thrombosis, or both.…”

Neuropathic Pain in Temporomandibular Joint Disorders: Case-Control Analysis by MR Imaging

“…These "false synapses" may fire and elicit-continuously and antidromically-the trigeminal spinal nucleus of the brain stem and might be a reasonable explanation of the neuropathic pain and sensory symptoms that affect some patients with TMJ-D (eg, headache, cervicalgia, toothache, ear sounds, painful cold, electric shocks, tingling, pins and needles, numbness, itching, hypoesthesia to touch, etc). [14][15][16][17] It is reported in the literature that, at the level of the brain stem, sensory neurons from the mandibular nerve share the same neuron pool as neurons from the maxillary, ophthalmic, and upper cervical nerves (cervical nerves I-III). This convergence of nerve fibers could explain how pain may be referred in different regions than in the dermatomal distribution of the mandibular nerve.…”