This review updates understanding and research on blepharospasm, a subtype of focal dystonia. Topics covered include clinical aspects, pathology, pathophysiology, animal models, dry eye, photophobia, epidemiology, genetics, and treatment.
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Blepharospasm should be differentiated from apraxia of eyelid opening. New insights into pathology and pathophysiology are derived from different types of imaging, including magnetic resonance studies.
Physiologic studies indicate increased plasticity and trigeminal sensitization. While botulinum neurotoxin injections are the mainstay of therapy, other therapies are on Andrew came into my office complaining of twitching eye horizon. Blepharospasm is a focal dystonia manifested by involuntary eyelid closure. This failure is called apraxia of eyelid opening, and is particularly common in Parkinson disease or other parkinsonian disorders such as progressive supranuclear palsy, but can be seen in isolation.
A diagnosis of apraxia is often made in error because selective contraction of the pretarsal portion of the orbicularis oculi can be responsible for eyelid closure. Unless this portion is injected specifically with BoNT, treatment will fail. There are, however, true cases of apraxia. Unequivocal proof of this depends on the demonstration by EMG of levator muscle inactivity despite an attempt of the patient to open the eyes. Because this is a specialized ophthalmologic procedure, the diagnosis remains largely based on careful clinical assessment and observation of delayed eye opening, with possible supplementation with EMG recordings from the pretarsal orbicularis oculi.
Surgical approaches with shortening of the levator tendon or a frontalis sling may help some patients.
The cortical control of eyelid closure is not well understood. Only relatively recently has there been the finding that a major source is the cingulate cortex M3 as well as lesser sources in primary motor cortex M1. New findings show a major input from the amygdala which presumably plays a role in behaviors such as emotional facial expressions.
While the primary dystonias are generally assumed to have their origin in pathology of the basal ganglia, this has not been proven.
In fact, the recent report of pathology in Oppenheim or DYT1 dystonia early onset autosomal dominant generalized dystonia shows pathology mainly localized to the brainstem. One study compared 16 patients and a matched set of healthy subjects. In another study of 11 patients, there was increased gray matter in the caudate head and cerebellum bilaterally and a decrease in the putamen and thalamus bilaterally.
Diffusion tensor imaging DTIanother MRI technique that assesses the integrity of white matter tracts, shows abnormalities in some forms of dystonia. Clearly, one of the next steps must be to look for histopathology in blepharospasm brains. Results are projected on A coronal and B axial slices of the study-specific averaged T1-image in a standard stereotactic space derived from all the 32 study participants. Reported from Etgen et al. There are many investigations of the focal dystonias using clinical neurophysiology, and much of this is likely relevant to blepharospasm since the focal dystonias are certainly related to each other.
Blink rates were compared during rest, conversation, and reading in 50 patients with blepharospasm and in healthy subjects. This reversal in the usual pattern of blinking suggests that conversation may reduce the excitability of eyelid closure and accounts for the common observation that patients with blepharospasm talk more than those without it.
The sensitivity and specificity of the two features number of blinks at rest and the pattern of blinking in discriminating patients and controls were found to be best with a resting blink rate above 27 blinks per minute. Patients with focal dystonias have sensory disorders as well as the more obvious motor dysfunction. Patients with focal hand dystonia have been shown to have deficits in tactile temporal discrimination, 18 and now this has been demonstrated for patients with blepharospasm as well.
There is considerable evidence that patients with dystonia exhibit increased plasticity. Linking these findings to the underlying pathology and to therapy remain challenges. Figure 2 Enhanced long-term potentiation-like plasticity of the trigeminal blink reflex circuit in blepharospasm. Magnitude of the R2 component of the blink reflex at baseline T0 and 30 minutes T30 and 60 minutes T60 following a session of high frequency stimulation of the supraorbital nerve timed to occur during the blink reflex.
Average data on the left and individual data on the right. Reprinted from Quartarone et al. PET neuroimaging with 18 fluorodeoxyglucose FDG was performed in 11 patients and a similar number of matched controls.
Areas with the most significant clusters of decreased glucose uptake Andrew came into my office complaining of twitching eye the left inferior cerebellum, thalamus, and inferior frontal Andrew came into my office complaining of twitching eye, ventral to the area of increased glucose metabolism.
A second study examined FDG PET in patients whose symptoms were suppressed by an injection of botulinum-A toxin in order to avoid a confound caused by sensory feedback from the dystonic movements although the intervention itself might be a confound.
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A significant increase in glucose metabolism was seen in the thalamus and pons in the patients. The inconsistent results of these studies make their interpretation unclear.
Functional MRI studies of blinking in patients with blepharospasm have not been done, but a study was done with whistling as part of a study of cranial dystonia previously also referred to as Meige syndrome. Overactivity of the primary sensory cortex is commonly seen with motor tasks in patients with focal dystonias, providing further evidence for the idea that dysfunction of the sensory system is important in the pathophysiology of this apparently motor disorder.
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Better animal models for blepharospasm would be useful in identifying new clinical approaches to blepharospasm. Consistent with the imaging studies describing abnormal cerebellar activity with blepharospasm, 13,24 recent animal models of dystonia indicate that the cerebellum might be a possible site of pathology.
An in vitro rat preparation has been used to look at the circuit between trigeminal input and facial nerve output, with the hope that the information learned will be useful in developing ideas about circuits that might become pathologic in blepharospasm. Trigeminal nerve stimulation at frequencies above 2 Hz produced rapid depression of the facial motoneuron EPSPs, reducing the gain of the sensorimotor loop and preventing the sensorimotor loop from creating uncontrollable spasms.
The investigators hypothesized that blepharospasm might arise because of an exceptionally high gain for the blink Andrew came into my office complaining of twitching eye loop created by a loss of this synaptic depression. A common explanation for the ocular discomfort of photophobia, often experienced by patients with blepharospasm, is that central visual neurons excite nociceptor centers in the ophthalmic region of the spinal trigeminal complex.
Another proposal is that the excessive pupil constriction evoked by bright lights activates nociceptors associated with the iris.
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To distinguish between different hypotheses for the neural basis of photophobia, Evinger personal communication developed an anesthetized rat model of photophobia. He utilized the observations from humans that trigeminal stimuli elicit blinks larger than spontaneous blinks and that people exhibit a higher spontaneous blink rate in the presence of lights reported as uncomfortable or painful.
Photophobia was quantified before and after lesioning both optic nerves in this model.
These data indicated that a significant portion of photophobia did not involve central visual pathways or pupil constriction. The simplest explanation of these results was that intraocular trigeminal nociceptors responding to retinal activity produced the majority of the photophobia.
This hypothesis can explain the occurrence of photophobia sometimes reported in blind patients. Many patients complain of dry eye, but objective findings are much less than the frequency of complaints. Dryness may have less to do with the amount of tears, and more to do with the makeup of the tear film and its dynamics. Whether any of these abnormalities are common Andrew came into my office complaining of twitching eye patients with blepharospasm and the extent to which these abnormalities may be etiologic are important issues needing further investigation.
Photophobia is a prominent complaint in patients with blepharospasm. Light is not only unpleasant, it also precipitates eyelid spasms. The visible spectrum of light is from about to nm, and frequent, but anecdotal, reports suggest that filtering the light may improve symptoms of blepharospasm. One important question is whether symptoms are better relieved by reducing light in a specific region of the spectrum or just the net flux. In one study designed to quantify light sensitivity in blepharospasm, 24 patients and 10 controls were evaluated with seven different chromatic lenses.
The light intensity tolerated by the normal subjects grew to 3. Reprinted from Herz and Yen 33 with permission from Elsevier, copyright Another case-controlled study compared 87 subjects in three groups: Light discomfort thresholds for subjects with blepharospasm were significantly lower compared with normal control subjects Andrew came into my office complaining of twitching eye similar to the migraine group. Both gray and FL tinted lenses improved light sensitivity thresholds in all groups.
There was no observed difference in the improvement in light sensitivity when the gray and FL tinted lenses were compared. In contrast to Herz and Yen, 33 the Adams et al. More work is necessary to understand the basis of the photophobia present in blepharospasm. The studies involving pathophysiology, animal models, dry eye, and photophobia suggest that sensitization of the trigeminal system plays a role in blepharospasm.
The increased plasticity of the blink reflex identified by Quartarone et al.
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As dry eye or ocular irritation sensitizes the trigeminal system, 37 the linkage between blepharospasm and ocular symptoms 38 points to the importance of trigeminal sensitization in blepharospasm. The similarity of light sensitivity exhibited by patients with blepharospasm and migraine 35 suggests that patients with blepharospasm share the trigeminal sensitization present in patients with migraine.
Age appears to be more of a risk factor Andrew came into my office complaining of twitching eye the development of blepharospasm than other types of focal dystonia. A validated questionnaire was administered to Italian patients with blepharospasm and age- and gender-matched control patients with hemifacial spasm particularly to assess ocular symptoms prior to the onset of blepharospasm.
In addition, the age at onset played a role since the association was stronger when the short-latency symptoms developed from 40 to 59 years of age.
In another multicenter case control study in Italy, prior coffee drinking and cigarette smoking habits were investigated in patients with blepharospasm, control patients with hemifacial spasm, and healthy control subjects.
The strength of the relationship between blepharospasm and coffee intake increased with the average number of cups of coffee per day, and there was a significant correlation between age at blepharospasm onset and number of cups per day. This finding is similar to what has been found in Parkinson disease 42 and remains unexplained.
Patients who develop blepharospasm may experience spread of the dystonia to other body parts.
One study followed patients with primary dystonias. Most spread occurred in the first 1 to 2 years after onset of blepharospasm, whereas the risk of spread was relatively constant over time in the other dystonias.
In another study, patients presenting with blepharospasm, 73 patients with cervical dystonia, and 24 patients with focal hand dystonia, all with 10 years or more of symptom duration, were compared. This greater risk of spread in blepharospasm was mainly evident in the first 5 years of the disorder. Similar findings were seen in a group of patients followed for a mean of 7.
A recent study re-evaluated the genetic influence in blepharospasm based on the examination of the first-degree relatives of 56 probands. Importantly, there was considerable phenotypic variability of dystonia within families.
It seems clear that all the focal dystonias are related to each other. Since polymorphisms of the genes encoding TorsinA DYT1 and the D5 dopamine receptor DRD5 have been associated with lifetime risk for focal dystonia, these genes were investigated in two independent cohorts of Italian and North American patients with blepharospasm. Although there is paucity of well-designed, double-blind, controlled studies, BoNT injections into the eyelids and eyebrows are now generally considered as the treatment of choice.
Myectomy should be a consideration. Deep brain stimulation DBS has been found to be effective in the treatment of generalized dystonia and cervical dystonia.
Recently, it was used to treat patients with disabling cranial dystonia, including blepharospasm, who have become refractory to other forms of therapy. Two early reports of pallidal DBS in patients with cranial dystonia showed a mild positive effect.
It is important to note that despite improvement in cranial-cervical dystonia, there was mild worsening of motor function in previously nondystonic body regions in four patients. 16 results Watch videos like: Gay XXX Andrew came into my office complaining of spasming eye. This, Gay movie His tight stud vagina spasms and blinks in. L. D. Britt, Phillip S. Barie, Andrew B.
Peitzman, Gregory Jurkovich. (most common) or anteriorly into the anterior chamber. Patients will present with blunt trauma to the globe. This causes inflammation of the iris and ciliary body and resulting ciliary spasm. Patients typically complain of pain, photophobia, and blurred vision.
Author: Arun Verma, MD; Chief Editor: Andrew A Dahl, MD, FACS more. Patients with a corneal abrasion typically complain of eye pain and an inability to open the aching discomfort from ciliary spasm and the foreign body sensation or The patient's history typically includes trauma to the eye Andrew came into my office complaining of twitching eye to.
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