First symptoms?

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Hi everyone! I am a new member and my english is not good, i'm just 26, a female. I have eyetwitch over 1,5 months, it only happens when i smile, pucker my lips, on upper lid and sometimes lower lid (come and go), Is that the early symptoms of hemifacial spasm? And what should i do if i dont have anything on MRI test? Botox or medicine can help? I so stressful b/c i will get mariage on this December! 

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    Hi, sorry you're having these problems.  It must be worrying especially being so young and with your marriage coming soon.  This does sound like the beginnings of Hemifacial Spasm.  The spasms or twitches do not have to be constant and in the early stages they will come and go.  It is a hard condition to diagnose and not all doctors understand it fully.  The MRI test may just say 'negative' or 'nothing abnormal' but this will not necessarily rule out HFS - it will just confirm that you do not have anything sinister like a tumour (which is rare).  I am going to append a piece from a medical study which talks about the diagnosis of HFS - it is technical and probably hard to understand (in any language) but it may help a bit. 

    Medicine does not really help HFS and it can have side effects which are worse than HFS.  If you need to get your face under control in time for your wedding then it might be worth having a small amount of Botox just around your eye area - do not let them give you a big dose or put any into the mouth or cheek area before your wedding, just in case it does not have a good result.  Botox can take 3 months to wear off so it's not something you really want to experiment with when you have a wedding coming up!  It might just be best to accept the symptoms and make sure your photographer takes lots and lots of photos to choose from.

    There is of course a potential cure for HFS if this is what you find you have.  This is surgery but it is a big operation and needs the most skilled surgeon (with precise experience of microvascular decompression for HFS).  But that is something to consider much much later.

    Hope this is helpful rather than frightening!  Here is the piece about diagnosing and treating HFS from the Scientific World Journal Volume 2014, article ID 349319:

    5. Diagnosis

    The diagnosis of HFS is made clinically. The “Babinski-2 sign,” “other Babinski sign,” or “brow-lift sign” is a physical exam maneuver that is positive when a patient lifts his/her eyebrow with ipsilateral eye closure, signaling the synchronized activity of the frontalis and orbicularis oculi muscle during HFS [42–44]. This technique has been shown in one study to have high sensitivity (86%), specificity (100%), and interrater reliability (92%) for HFS diagnosis [45].

    EMG, MRI, and computerized tomography (CT) are used to confirm the diagnosis and differentiate primary from secondary HFS. Of these modalities, T2-weighed MRI sequences and high resolution fast imaging employing thin section steady-state free precession MR images are most commonly used to display possible vascular compressions [21]. Fusion MR imaging that combines steady-state MR imaging and three-dimensional time-of-flight MR angiography has been shown to assist in describing patient-specific anatomy at the root exit zone of the facial nerve [46]. EMG can also be useful to differentiate HFS from other abnormal facial movement disorders; in HFS, spontaneous, high-frequency synchronized firing is seen on EMG [3]. Additional diagnostic techniques such as a CT angiogram are useful for microsurgical planning. A recent study also suggested that the hemodynamic changes may be detectable using color-duplex ultrasound, showing a higher mean blood flow velocity in PICA and AICA arteries on the HFS side compared to that of the contralateral face [47]. An analysis using three-dimensional MR volumetric analysis found that HFS patients have lower posterior fossa CSF volumes compared to that of matched controls, suggesting that smaller posterior fossa CSF space may be an HFS risk factor [48].

    All these diagnostic techniques help differentiate HFS from other craniofacial dyskinesias such as blepharospasm (BSP), tic disorders, myokymia, and synkinesis in addition to other disorders such as partial motor seizures, craniocervical dystonia (Meige syndrome), tardive dyskinesias (TD) and neuromyotonia. Other conditions such as psychogenic HFS, facial myoclonus, oromandibular dystonia, and hemimasticatory spasm can masquerade as HFS, resulting in diagnostic difficulty [34]. One case of moyamoya disease presented as HFS and was identified due to facial nerve compression with compensatory posterior circulation vessel enlargement [49]. In addition, psychogenic HFS was found in 2.4% of patients evaluated for HFS in one study and can lead to unnecessary medical and/or surgical intervention [50].

    Comorbidity between HFS and other craniofacial dyskinesias can occur. Trigeminal neuralgia (TN) is irritation of the trigeminal nerve that causes facial pain. It can present concurrently with HFS in a syndrome called tic convulsif. Studies have shown that HFS can follow Bell’s palsy, which is facial paralysis from dysfunctional facial nerve caused by brain tumor, stroke, myasthenia gravis, and Lyme disease [34]. HFS has also been reported to occur as a result of facial nerve demyelination in multiple sclerosis patients.

    6. Medical Treatment

    The standard medical treatment for HFS is botulinum neurotoxin (BoNT) injections. Having been used since the early 1980s, BoNT injections provide low-risk symptomatic relief in 85% of HFS patients, making it the treatment of choice for patients with high anesthetic risk and those who refuse surgery [21]. One study suggested that BONT-A also helped improve hemifacial spasm-related headaches [8].

    BoNT’s mechanism of action is to block calcium-mediated release of acetylcholine at the synaptic junction. Two serotypes are available: BoNT-A and BoNT-B, as well as four different commercial formulations: abobotulinumtoxinA, onabotulinumtoxinA, incobotulinumtoxinA, and rimabotulinumtoxinB [51]. After injection, BoNT is cleaved by trypsin into heavy and light chain components [52]. At this point, the BoNT toxin is internalized into presynaptic nerve terminals, where the heavy chain binds synaptic vesicle protein 2, trisialoganglioside 1b, and synaptotagmin-1 [53]. The light chain then binds to the SNARE complex and cleaves target proteins such as synaptosomal-associated proteins of 25?kDa (SNAP-25) and synpatobrevin-2 to prevent exocytosis of neurotransmitters from the presynaptic terminal, leading to muscle paralysis [54].

    BoNT-A is the primary serotype used for HFS treatment. BoNT-A injections occur in several sites in the pretarsal and preseptal portions of the facial nerve and are effective with a mean onset of action of 3 to 5 days. In one longitudinal multicenter center study, the effectiveness of BoNT-A in relieving HFS symptoms remained unchanged in the first and tenth year with patients needing statistically similar doses [55]. However, the injections must be repeated every 3 to 6 months. Tolerance can develop in some cases, but the treatment is generally well tolerated. Local complications of these injections include ptosis, blurred vision, and diplopia that may improve after days to weeks [14]. Repeated injections also can cause atrophy of target muscles, which may lead to injection of the contralateral face for cosmetic reasons [54]. Despite the effectiveness and low complication rate of BoNT-A, the need for repeated injections incurs a high economic cost and provides only symptomatic relief. Comparatively, BoNT-B is less commonly used. In an open-label single dose study, BoNT-B serotype was also shown to be well tolerated with 40% of subjects responding to treatment [56].

    Pharmaceuticals such as anticonvulsants and GABAergic drugs may be used as alternative to BoNT injections. These drugs are generally less effective compared to BoNT at treating HFS. No controlled studies have found demonstrated long-term effectiveness of these medications, limiting their treatment utility. However, they can be used for symptomatic relief in early HFS patients who have mild and infrequent symptoms as well as patients who decline BoNT injections and/or surgical intervention. 

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    Hi dear! I am older than you by 2 years since I just turned 28 last month. I also have HFS and im on my medication right now. I've been to my neuro three times for there is a change on the medication he gave me. 

    As of this time, HFS is still there but I noticed it was minimized. I remember before my medication, HFS happens majority of the day. But now, it was minimized. 

    I also do some research, and many forums i read was the use of SPZM. I ordered online and still im waiting for it to come so i may try it. 

    I pray for all of us so this HFS may disappear. 



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  • Posted

    Hi just get married because your beauty come from within in x this could be HFS or other things you need to see your gp x
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  • Posted

    Too early to say. Take my advice, do not research about hfs or for that matter any medical problem on internet. Go to your doctor instead.
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