[Secondary blepharospasm, analysis and pathophysiology of blepharospasm. French translation of the article]. / Blépharospasmes secondaires, analyse et réflexion sur la physio-pathogénie du blépharospasme.

PURPOSE: To localize the brain structures involved in blepharospasm. MATERIALS AND METHODS: This is a retrospective consecutive series of brain MRI's of patients with secondary blepharospasm whose immediate past medical history included cerebrovascular accident or head trauma. RESULTS: Six patients, including 4 with CVA with ischemic or hemorrhagic lesions of the thalamus and caudate nuclei and 2 with head trauma with contusive sequellae to the tectal plate and frontal cortical and cerebellar atrophy. CONCLUSION: According to the literature, brain lesions associated with blepharospasm involve mainly the thalamus, head of the caudate nucleus, corpus striatum, globus pallidus, internal capsule, cerebral cortex and cerebellum. This study demonstrates that blepharospasm is associated with a lesion of a complex neural network - cortex-thalamus-globus pallidus-cortex - and does not correspond to a single, unique lesion. This network is connected with ascending and descending sensory-motor pathways and motor nuclei.

[Hemifacial spasm. Etiology and management]. / Spasmes hémifaciaux. Étiologies et conduite à tenir.

INTRODUCTION: Hemifacial spasm (HFS) is an involuntary contracture of the facial muscles innervated by the ipsilateral facial nerve. We studied the etiology of these HFS. MATERIALS AND METHODS: This retrospective study included 233 patients with HFS who came to the ophthalmologist for quarterly botulinum neurotoxin A injection. Of these, we analyzed the 198 patients for whom MRI scans were performed. We recorded patient clinical data and clarified the etiology of their HFS. RESULTS: The 198 patients (62.6% women) had a mean age of 55.7±14years. An etiology was found in 52.5% of cases. In 34.5% of HFS, MRI revealed vascular compression where the facial nerve emerged from the brainstem. We specify the arteries involved. Brain tumors accounted for 1.5% of cases. MRI was normal in 64.5% of cases. In these secondary cases of HFS, we found 8.5% peripheral facial palsy, 4% post-traumatic HFS and 4% secondary to an eye injury. Stress was found in 17% of patients. DISCUSSION AND CONCLUSION: This study illustrates the need for MRI with attention to the posterior fossa in the work-up of HFS in order to identify primary HFS associated with vascular compression of the facial nerve and to rule out a rare but serious posterior fossa tumor. The treatment of HFS is based on quarterly injections of botulinum neurotoxin/A (NTBo/A), the three brands of which have market approval. The injection pattern and frequency is customized according to the results. In cases of insufficient response to injections of NTBo/A, neurosurgical microvascular decompression may be considered for cases of primary HFS.

Secondary blepharospasm, analysis and pathophysiology of blepharospasm.

PURPOSE: To localize the brain structures involved in blepharospasm. MATERIALS AND METHODS: This is a retrospective consecutive series of brain MRI's of patients with secondary blepharospasm whose immediate past medical history included cerebrovascular accident or head trauma. RESULTS: Six patients, including 4 with CVA with ischemic or hemorrhagic lesions of the thalamus and caudate nuclei and 2 with head trauma with contusive sequellae to the tectal plate and frontal cortical and cerebellar atrophy. CONCLUSION: According to the literature, brain lesions associated with blepharospasm involve mainly the thalamus, head of the caudate nucleus, corpus striatum, globus pallidus, internal capsule, cerebral cortex and cerebellum. This study demonstrates that blepharospasm is associated with a lesion of a complex neural network - cortex-thalamus-globus pallidus-cortex - and does not correspond to a single, unique lesion. This network is connected with ascending and descending sensory-motor pathways and motor nuclei.