Hemifacial spasm (HFS) is a neuromuscular movement disorder characterized by brief or transient involuntary contractions of the muscle activated by the ipsilateral facial nerve (Cranial Nerve VII).
In most cases, the orbicularis oculi muscle region experiences involuntary spasms, which subsequently spread to other areas of the affected half of the face.
Epidemiology
The prevalence of HFS appears to be more common in nearly some of the Asian populations than in Caucasians. The age group of 40-50 years is more vulnerable to this disease.
Anatomy
Pathophysiology
The primary cause of hemifacial spasm is an abnormal blood vessel that compresses the facial nerve as it exits from the brainstem. The nerve is surrounded only by an arachnoidal membrane.
Individual fascicles are not connected by connective tissue septa, which creates a cross-over between central and peripheral myelination, resulting in increased susceptibility and thus the compression-like stimulation.
Etiology
In the root exit zone of the brain stem, ectopic and ephaptic excitation occurs. The latter transfers the impulse to neighboring nerve fibers, and the former develops spontaneous neural impulses in the compression area.
Rare causes of hemifacial spasm include space-occupying lesions in the cerebellopontine angle such as benign and malignant tumors (epidermoid, meningioma, lipoma, hematoma), cerebral abscess, arachnoidal cysts.
Genetics
There is an unclear hereditary pattern usually because of autosomal dominant minimal specificity. The age of onset is variable but frequently observed in the early years of life.
Prognostic Factors
Elevated blood pressure is considered a risk factor for HFS as it causes atherosclerosis which may increase the narrowing of vessels and result in subsequent facial nerve compression. In contrast, compression of the vessel also causes elevated blood pressure.
Hemifacial spasm (HFS) is a neuromuscular movement disorder characterized by brief or transient involuntary contractions of the muscle activated by the ipsilateral facial nerve (Cranial Nerve VII).
In most cases, the orbicularis oculi muscle region experiences involuntary spasms, which subsequently spread to other areas of the affected half of the face.
The prevalence of HFS appears to be more common in nearly some of the Asian populations than in Caucasians. The age group of 40-50 years is more vulnerable to this disease.
The primary cause of hemifacial spasm is an abnormal blood vessel that compresses the facial nerve as it exits from the brainstem. The nerve is surrounded only by an arachnoidal membrane.
Individual fascicles are not connected by connective tissue septa, which creates a cross-over between central and peripheral myelination, resulting in increased susceptibility and thus the compression-like stimulation.
In the root exit zone of the brain stem, ectopic and ephaptic excitation occurs. The latter transfers the impulse to neighboring nerve fibers, and the former develops spontaneous neural impulses in the compression area.
Rare causes of hemifacial spasm include space-occupying lesions in the cerebellopontine angle such as benign and malignant tumors (epidermoid, meningioma, lipoma, hematoma), cerebral abscess, arachnoidal cysts.
There is an unclear hereditary pattern usually because of autosomal dominant minimal specificity. The age of onset is variable but frequently observed in the early years of life.
Elevated blood pressure is considered a risk factor for HFS as it causes atherosclerosis which may increase the narrowing of vessels and result in subsequent facial nerve compression. In contrast, compression of the vessel also causes elevated blood pressure.
Hemifacial spasm (HFS) is a neuromuscular movement disorder characterized by brief or transient involuntary contractions of the muscle activated by the ipsilateral facial nerve (Cranial Nerve VII).
In most cases, the orbicularis oculi muscle region experiences involuntary spasms, which subsequently spread to other areas of the affected half of the face.
The prevalence of HFS appears to be more common in nearly some of the Asian populations than in Caucasians. The age group of 40-50 years is more vulnerable to this disease.
The primary cause of hemifacial spasm is an abnormal blood vessel that compresses the facial nerve as it exits from the brainstem. The nerve is surrounded only by an arachnoidal membrane.
Individual fascicles are not connected by connective tissue septa, which creates a cross-over between central and peripheral myelination, resulting in increased susceptibility and thus the compression-like stimulation.
In the root exit zone of the brain stem, ectopic and ephaptic excitation occurs. The latter transfers the impulse to neighboring nerve fibers, and the former develops spontaneous neural impulses in the compression area.
Rare causes of hemifacial spasm include space-occupying lesions in the cerebellopontine angle such as benign and malignant tumors (epidermoid, meningioma, lipoma, hematoma), cerebral abscess, arachnoidal cysts.
There is an unclear hereditary pattern usually because of autosomal dominant minimal specificity. The age of onset is variable but frequently observed in the early years of life.
Elevated blood pressure is considered a risk factor for HFS as it causes atherosclerosis which may increase the narrowing of vessels and result in subsequent facial nerve compression. In contrast, compression of the vessel also causes elevated blood pressure.
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