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Types of Brain Tumors
Vascular Neurosurgery. Samer S. Compression of the facial nerve while it course through facial canal, especially the narrow labyrinthine segment, is the most acceptable theory. The compression has been demonstrated in MRI scan with facial nerve enhancement [ 12 ]. Any inflammatory, demyelinating, and ischemic or compressive process in this area may impair the neural conduction. Other viruses include Mumps virus, cytomegalovirus, and HIV. Other suggested theories include autoimmunity, mycoplasma infection, inflammation, microvascular disease such as diabetes mellitus, and many other mechanisms.
It is apparent that none of these theories stands on a solid base. The paralysis must include the upper and lower aspects of the face, otherwise, if it involves the lower portion of the face, a central cause supranuclear , such as stroke, should be suspected. If the onset of the facial paralysis is insidious, associated with weakness of the contralateral side, or there is a preceding history of trauma or infection, other causes of facial paralysis must be strongly considered.
In addition to the sudden onset of unilateral upper and lower facial muscle paralysis, the patient may have hyperacusis, posterior auricular pain, otalgia, incomplete eye closure, excessive salivation, and taste disturbances. Many patients report numbness on the affected side. Whether this numbness is due to the involvement of trigeminal nerve or lack of movement of facial muscle is not clear.
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Ocular pain, epiphora or decreased tearing, and blurred vision are other possible associated symptoms. The patient should be examined in details for full neurological examination, any skin lesion, ear or eye problem, and parotid diseases. Hearing defects and facial paresis are the most common presenting features. The most commonly identified tumor are schwannomas. Facial nerve schwannomas are benign tumors, which arise from Schwann cells. They mostly occur sporadically; some occur as a part of genetic syndromes as neurofibromatosis types 1 and 2.
The facial nerve is the third common site for intracranial schwannomas. The patient usually presents with sudden onset or progressive facial weakness with or without conductive or sensorineural hearing loss, tinnitus, vertigo, facial pain, hemifacial spasm, facial palsy, and otalgia. Most of these tumors present with facial palsy with or without hearing defects. It is a segmental myoclonus of muscles innervated by the facial nerve. Gowers first described it in It affects 11 per , of the population mostly in the fifth and sixth decade of life with a slight female predominance.
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The majority of cases are unilateral, although bilateral involvement might occur rarely in severe cases. It generally starts as brief clonic movements of the orbicularis oculi that spread over the years to other facial muscles corrugator, frontalis, orbicularis oris, platysma, and zygomaticus , and it may become more sustained with time. HFS is characterized by progressive involuntary clonic or tonic movements of the muscle supplied by the facial nerve. It typically started in the orbicularis oculi muscle and progressively extends to involve the other facial muscle, involving the platysma muscle in severe cases.
Most of the cases persist during sleep, and some patients report clicking sound in the ear, which presumed to be due to contraction of the stapedius muscle. In severe cases, impairment of vision might occur because of severe spasm of the orbicularis oculi muscle. The symptoms are usually exaggerated by psychological tension and speech. The main differential diagnosis of HFS includes blepharospasm occur bilaterally symmetrically , oromandibular dystonia sustained contraction of the lower part of the face, mouth, mandible and maxilla, tongue and pharynx , facial nerve tic complex coordinated multifocal movement that switches between the right and left sides of the face , hemimasticatory spasm painful contractions of the muscles of mastication , focal seizures, and synkinesias after facial nerve paralysis activation of several muscles innervated by the facial nerve.
The editor of this book is afflicted by right-sided HFS started at the age of 45; unfortunately, vascular decompression failed to resolve the problem.
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A Spasm of the right orbicularis oculi and right facial muscle and B spontaneous resolution of the spasm. The underlying cause of hemifacial spasm in most cases is an ectatic or atypically aberrant blood vessel, which compresses the facial nerve at the place where it exits the brain stem. This area is the most susceptible part of the facial nerve to external stimuli since it ensheathed only by an arachnoidal membrane without the epineurium. Furthermore, this area represents the transition zone between central oligodendroglial cells and peripheral Schwann cells myelinations, and there is no connective tissue septa that traverse the individual fascicles.
In the majority of cases, inferior posterior cerebellar artery or the inferior anterior cerebellar artery is the cause for vascular compression. Rarely, vertebral artery or a combination of these arteries is responsible for this compression. Very rarely, a vein might be the cause. These investigations are useful also to exclude pathological changes in the cerebellopontine angle such as tumors or brain stem lesions.
A high-resolution, T2-weighted sequence is particularly useful in demonstrating vascular compression. The therapeutic options for HFS are variable ranging from simple applications of heat to pharmacological treatment carbamazepine, clonazepam, baclofen, and gabapentin and botulinum injections to microvascular decompression surgery.
The response to medications, in general, is poor and not sustained and thus is devoted to milder cases. The major advantages of BTX are that it is a noninvasive technique and can be done in an outpatient setting. The only curative therapeutic option is microvascular decompression of the facial nerve by placing a Teflon sponge between the vessel and the brain stem. Additionally, postoperative complications including temporary or permanent hearing impairment and permanent facial paralysis may occur in up to 8 and 0. Involvement of the lower face by spasm is not uncommon, and the patient might be functionally blind as the eyes might be closed most of the day.
The cause of the blepharospasm is thought to be central, yet the exact mechanism is not known. Treatment options include selective destruction of facial nerve branches that innervate the orbicularis oculi muscle, inducing paralysis of orbicularis oculi muscle by BOTOX, and pharmacological therapy by anticholinergics drug Artane , benzodiazepine clonazepam , GABAB receptor agonist baclofen , anticonvulsant levetiracetam , and many other drugs [ 25 ]. In addition to a detailed history and clinical examination, investigations are an essential part of the workup of patients with facial nerve disorders.
Still, there are controversies about the appropriate investigations that are needed for patients present with facial nerve disorders. The most commonly used investigations include:. These tests used to detect any associated hearing defect and diminished stapedial reflex paresis of the stapedial branch of the facial nerve.
Brain stem auditory evoked response BAER in particular is effective in detecting retrocochlear lesion. These tests are not used routinely unless there are multiple cranial nerve palsies [ 26 , 27 ]. Imaging studies play an important role in the evaluation of facial nerve disorder. MRI is especially helpful in recognizing brain stem pathology, and high-resolution CT scan is helpful in identifying bony abnormalities of the intratemporal facial nerve like congenital anomalies, trauma, and cholesteatoma.
MRI is especially helpful in the detection of soft tissue abnormalities around facial nerve as in neoplasms, inflammatory processes, and hemifacial spasm. Recently, facial nerve ultrasound and diffuse tensor tractography three-dimensional reconstruction of facial nerve using MRI are used to identify cranial nerve fiber displacement by vestibular schwannomas [ 28 , 29 ].