Devi Budhathoki, a woman from Nepal, along with three of her children, suffer from a very rare disease called Congenital Hypertrichosis Lanuginosa which. Anisocoria. Causas. 2 de #DrDomingoRománOviedo #Oftalmólogo # Microcirujano. /o injuria cerebral traumatica entre las causas que produje- ron la muerte. 1 La anisocoria (diferencia en el diámetro pupilar de am- bos ojos >1 mm) se.
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Oculosympathetic paresis, historically known as Horner sydrome, classically results in a triad of ptosis, miosis, and anhydrosis on the affected side. Any interruption or insult to any part of the sympathetic pathway to the eye can result in these classic findings. There are many possible etiologies along the three-neuron pathway, however, a few potentially life threatening cahsas must always be ruled out, especially in acute presentations.
One life threatening etiology, in particular, to rule out is of aniisocoria carotid artery dissection ICAD.
The patient was started on oral anticoagulants and oral steroids. This case report reviews the clinical findings, diagnoses, treatment, and management of patients with Horner syndromes secondary to ICAD. Se suministraron a la paciente anticoagulantes y esteroides orales. Horner syndrome, commonly also referred to as oculosympathetic paresis, was first described by three American army physicians in in a causqs who was shot through the throat. The miotic pupil in Horner syndrome occurs secondary to the unopposed innervation of the parasympathetic system, anisocpria the ptosis and anhidrosis findings are induced by the lack of sympathetic innervation in general.
Etiologies are vast and range anizocoria benign to life-threatening causes such as malignancies or internal carotid artery dissections. Most common causes of Horner syndrome.
She denied any recent trauma.
Fones de Ouvido Podem Causar Perda Auditiva e Zumbido
She reported she did anisocorja to stop mid-race to bend over and tie her shoes. Her medical history was positive only for seasonal allergies and a history of a concussion 3 years prior after falling off of her bike. The patient reported no significant allergy contributory to her presentation. The patient’s family ocular history was entirely unremarkable. Her extraocular motilities were noted to have full range of motion in both eyes OU with no signs of restriction nor any complaints of diplopia.
Confrontational visual fields were full-to-finger-count OU. Pupils were measured in light and dark conditions. Both pupils reacted briskly to light and there were no signs of any afferent pupillary defect OU.
There was no sign of light and near dissociation in either eye. Her accommodative pupillary responses were normal OU as well. Adnexal examination did reveal subtle upper lid ptosis OS when compared to the OD. No signs of ipsilateral anhydrosis were found nor reported by the patient. The slit lamp biomicroscopy exam was cauas unremarkable OU.
The patient’s dilated fundus exam revealed that her causax poles and peripheral retinas were aniscooria within normal limits.
Cup-to-disc ratio was 0. Common differential diagnoses to consider are listed in Table 2. Photo of subtle lid ptosis OS and subtle anisocoria upon initial presentation.
Common differential diagnoses of pupil and ptosis abnormalities not an exhaustive list and in no particular order. Based on ccausas clinical presentation, the patient was diagnosed with a painful left-sided, partial Horner syndrome of unknown etiology based on the anisocoria and ptosis OS findings, however carotid artery dissection was highly suspected given the painful nature of presentation. Four days later the Anisocorla notified our clinic that the imaging studies had, indeed, revealed a carotid artery dissection of the distal half of the left internal carotid artery ICA at the level of approximately cervical vertebrae C3.
One week later the patient returned for follow-up.
She reported she was feeling better but that the headache was still present, although not as severe as the previous week. She reported her ptosis was still evident, but improved, and that she had noticed her pupils were now consistently the same size.
Her extraocular motilities were again full-range-of-motion with no signs of restriction OU. Confrontational visual fields were also again full-to-finger-count OU.
Anisocoria – Wikipedia
Accommodative pupillary response was normal at this visit as well. The remainder of the eye exam was stable and unchanged from previously. The patient was told to follow up with her PCP and neurologist as directed and was told to follow up at our clinic in 2—3 months for follow-up. The patient returned for follow-up 3 months later.
The neurologist discontinued the hydrocodone and instead gave the patient oral gabapentin to manage her ongoing pain secondary to the ICAD. The patient reported her signs and symptoms had dramatically improved over the past few months and that she had not noticed any lingering ptosis or pupil abnormalities.
She reported her neck pain and associated headaches had lessened in overall frequency as well. Extraocular motilities were again full-range-of-motion with no signs of restriction OU. Confrontational visual fields were still full-to-finger-count OU. Accommodative pupillary responses were normal OU as well.
The rest of the anterior segment and dilated fundus exams were completely unremarkable OU and consistent with her previous exams. The patient was instructed to follow up with her neurologist and PCP as directed for her ongoing care, and to follow up with our clinic in 6 months to monitor her ocular signs and symptoms.
Repeat MRA 2—3 months later of left carotid artery dissection with vast improvement of lumenal patency. A thorough understanding of the oculosympathetic pathway is critical in understanding and detecting the underlying pathophysiology of Horner syndrome. The oculosympathetic pathway has a long and tortuous route from the hypothalamus prior to innervation of the ocular structures.
It has three neuronal chains: First order neurons originate in the hypothalamus and descend anisociria the brainstem where it terminates at the approximate level of T1 known as the ciliospinal center of Budge—Waller.
The second order neuron preganglionic exits the spinal cord, travels in the sympathetic abisocoria over the apex of the lung, and ends approximately near the bifurcation of the common carotid artery located at the lower mandible of the jaw, at the superior cervical ganglion.
The third order neuron postganglionic leaves the superior cervical ganglion, ascends as a plexus surrounding the internal carotid artery to the cavernous sinus, jumps off onto the abducens nerve CN VI for a short course, then onto the ophthalmic branch of the trigeminal nerve CN V where the fibers travel via the nasociliary nerve through the superior orbital fissure. The fibers then pass through, but do not synapse on the ciliary ganglion. Thus, an incomplete or partial Horner syndrome will occur with the absence of anisociria which was the case with our patient.
ICAD is reported to have an incidence of 2. ICAD are typically classified as either spontaneous or traumatic. Motor vehicle accidents are the most common cause of traumatic cases. The anosocoria of action is best understood on a histological level of blood vessel anatomy.
Typically, injuries causing an ICAD involve hyperextension and rotation of the neck. The lamina intima, being the most inelastic layer of arterial vessels, tears under the forces of hyperextension and rotation.
The blood in the Anisoxoria lumen then invades the space in the causad wall creating a hematoma which typically dissects more distally, secondary to the direction of blood flow in the artery, than proximally, as well as for variable distances in the arterial wall. A history of hypertension, smoking, and oral contraceptive use have been shown to be more prevalent in ICAD patients, however atherosclerosis is distinctly uncommon in patients with ICAD.
Hydroxyamphetamine is the second drug used with Horner syndromes and has been used historically to localize the lesion after a positive cocaine test. If the pupil does not dilate with hydroxyamphetamine then the lesion is postganglionic. However, if dilation does occur then the lesion is assumed to be preganglionic in nature.
A newer pharmacologic alternative has recently been suggested. There has been an increasing number of anisocoriq of both 0. Historically, conventional angiography has been the gold standard for imaging ICAD’s. An additional topic that surfaces fairly frequently in the literature is that of imaging ICA’s with duplex ultrasound given its lower cost.
In our patient’s case, in-office pharmacologic testing was deferred given the obvious diagnosis of an acute-onset Horner syndrome based upon the patient’s history, presenting signs, and her painful symptoms which necessitated an urgent diagnostic investigation. Given the acute and rapid onset of her signs and symptoms, the lack of time necessary for denervation hypersensitivity to appropriately develop would have made apraclonidine or additional pharmacologic testing difficult to rely on.
The patient’s Horner syndrome, as discussed previously, was caused by an ICAD most likely associated with her history of running a short race a few days earlier. The process of her stopping mid-race to bend down and tie her shoe may have set off her cascade of signs and symptoms. Cauass she bent down, her neck most likely hyperextended and rotated to some degree, which stretched the lamina intima layer of the carotid artery leading to a small defect in the arterial wall.
In support of this, a literature review clearly supports cases of ICAD secondary to trivial trauma and sporting events such as in this case.
It is difficult to determine if she, indeed, had an underlying inherent structural defect in the wall of her carotid arteries, secondary cauaas such systemic conditions as previously mentioned in this article. If she did, this would have increased her risk of ICAD which may have been aggravated by her short marathon race and bending over to tie znisocoria shoes.
Nonetheless, she is being watched closely by our clinic, her PCP, and her neurologist.
Her long-term prognosis for a full recovery with no restrictions or residual complications from her ICAD is very good given her anisocoriz age and healthy lifestyle anisocotia general. She will continue to be ahisocoria closely until her signs and symptoms have proven consistently stable in nature. Horner syndrome secondary to an ICAD is a rare, but well-reported finding in ophthalmological literature. Appropriate management of these patients typically results in very anisocoriia prognoses and outcomes for the vast majority.
Emergent MRI of the entire oculosympathetic pathway should also be considered in acute Horner sydnrome without clear etiology to rule out other potential aniwocoria causes, in addition to ICAD. Likewise, underlying systemic conditions should be investigated in all patients anusocoria ICAD via the patient’s primary care provider to rule out any further inherent structural defects or other potential complications which may be managed appropriately to prevent any possible future medical complications.
The author has no financial or other relationships that might lead to conflict of interest. National Center for Biotechnology InformationU. Journal List J Optom v. Published online Jun 9. Author information Article notes Copyright and License information Disclaimer. Received Feb 26; Accepted Apr Abstract Oculosympathetic paresis, historically known as Horner sydrome, classically results in a triad of ptosis, miosis, and anhydrosis on the affected side.
Introduction Horner syndrome, commonly also referred to as oculosympathetic paresis, was first described by three American army physicians in in a soldier who was shot through the throat.
Table 1 Most common causes of Horner syndrome. Open in a separate window. Table 2 Common differential diagnoses of pupil and ptosis abnormalities not an exhaustive list and in no particular order.