Right Facial Hemispasm caused from Neck Problems
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I have had facial hemispasm for 5 years now. After researching the internet for causes and treatment, I stumbling upon this forum and was reading multiple posts about 4 years ago in which a person named "windhur" posted his discoveries which helped him. He concluded that his neck was causing the problem. I was thrilled to hear this as I was telling my doctors that I am 95% sure my neck is contributing to this facial spasm. I had three whiplash injuries to my neck, a right shoulder that dislocates anteriorly for the last twenty years and extreme neck tightness especially the right side. I have started doing stretches with heat and massage to the neck area concentrating on the right side with postural excercises to correct bad posture. (text neck ). I have had no botox treatments. I have also starting wearing special glasses that filter outs the harmful rays of light because of sensitivity to lights and noise (I also suffer from migraine with dizziness) and have had a 80% improvement in my hemispasm. I am concluding for myself that my neck is playing a huge part in this disorder. I would love to get in touch with this person by the name of "Windhur" who also stated that the neck played a part in his disorder and for any feedback since this persons postings and to see the progess today. I would love to hear from others with this disorder and their treatment.
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Roseann rosjane
Posted
Hi Rosjane, I recall posts by 'Windhur' or 'Windhurt' possibly. You will probably find them by trawling through the other threads under the main heading of Hemifacial Spasm. Hemifacial spasm can be caused by the primary cause (a compression of the 7th cranial nerve) or secondary causes (for example trauma or a even a tumour that may have damaged the same nerve. There is some useful research online about these two causes - I think Dr Raymond Sekula et al explain it well in the Scientific World Journal 2014 (Vol 349319). I will try to cut and paste a section from this research below - yes, it's pasted OK! If you need further information then it may be a good idea to join the Facebook Group (Hemifacial Spasm International Support Group) - that group has lots of helpful people and probably the best information around.
Here's the piece from Section 4 - Etiology:
'The etiology of HFS can be divided into two types: primary and secondary. Primary HFS is defined by vascular compression of the facial nerve root entry zone in the posterior fossa [30, 31]. Implicated arteries include the anterior inferior cerebellar artery (AICA), posterior inferior cerebellar artery (PICA), and vertebral artery (VA). Anatomic variations in vasculature such as lateral deviation of one or both vertebral arteries occurred on the ipsilateral side of HFS in 86.4% cases, making these variations a HFS risk factor [32]. The pattern of neurovascular compression can be divided into six different categories: (A) loop type, where the vascular itself creates the compression, (B) arachnoid type, where arachnoid trabeculae between the vessel and brainstem cause the vessel to tether to the nerve, (C) perforator type, where the perforating arteries from the compressing vessel tether the vessel to the brainstem, (D) branch type, where the nerve is caught between the compressing vessel and its branches, (E) sandwich type, where the nerve is sandwiched between two different vessels, and (F) tandem type, where one vessel compresses another vessel that compresses the nerve [33]. Multiple vessel compressions have been observed in 38% of HFS cases [23]. However, many patients present without an identifiable etiology [34]. Some studies have shown a higher prevalence of hypertension in patients with primary HFS compared to patients with other neurological diseases [1, 35, 36]. The association suggests that hypertension leads to arterial vessel ectasia and contributes to neurovascular compression of the facial nerve [1].
Secondary HFS occurs with damage anywhere along the facial nerve from the internal auditory canal to the stylomastoid foramen [30]. Cases of secondary HFS have been linked to cerebellopontine angle (CPA) tumors and vascular malformations with other case linked to facial nerve trauma, demyelinating lesions, and vascular insults [34]. CPA tumors occur rarely; in a study of 2,050 HFS cases, only nine patients had HFS that was attributable to CPA tumors, which included two vestibular schwannomas, five meningiomas, and two epidermoid tumors [37]. Mechanisms of HFS in this study also differed with six cases identifying offending vessels as well as individual cases of tumor encasement of the facial nerve, hypervascular tumor compression of the facial nerve, and a large tumor compressing the brain stem causing contralateral facial nerve compression [37]. Young onset HFS has been linked to Chiari type I malformations, which has been attributed to these patients’ narrow and shallow posterior fossa that crowd cranial nerves and vascular structures inside the cerebellopontine angle cistern [38, 39].
Collectively, these underlying issues of secondary HFS are thought to cause neural dysfunction and/or irritation of the facial nerve pathway [40]. Hearing loss, weakness of upper and low facial muscles, and preferential involvement of the orbicularis oculi and frontalis muscle were significantly more common in secondary HFS compared with primary HFS cases [7]. In a study of 252 patients, 78.5% presented with primary HFS whereas 21.5% presented with the secondary form [7]. Additional studies support that primary HFS is approximately 4 times more common than secondary HFS [30, 41].'
Hope this may have helped a bit!
rosjane Roseann
Posted
Thank you so much. You reply was a wealth of information. I will do further trawling to find Windhurt and I plan on joining the facebook group. That scientific world article was an interesting read.