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A Brief Review on Anisocoria
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We have compared the diagnostic ability of different concentrations of 0.125% and 0.0625% dilute pilocarpine for detecting denervation supersensitivity in unilateral Adie’s tonic pupil. This retrospective, observational, case–control study involved 117 subjects, consisting of 56 patients with unilateral Adie’s tonic pupil and 61 controls with other causes of unilateral dilated pupils. Subjects underwent the dilute pilocarpine test with one of the two concentrations, 0.125% or 0.0625%. Pupillary light reflex was recorded with a dynamic pupillometer at baseline and at 30–40 min after instilling one of the two concentrations of dilute pilocarpine. Diagnostic accuracy of two different concentrations of the dilute pilocarpine test, 0.125% group versus 0.0625% group, were compared by area under the receiver operating characteristic curve (AUC). Diagnostic ability of the dilute pilocarpine test for detecting denervation supersensitivity in unilateral Adie’s tonic pupil was significantly better in the 0.0625% group than in the 0.125% group (AUC = 0.954 vs. 0.840, respectively, P = 0.047). In the 0.0625% group, the change in maximal pupil diameter of ≥ 0.5 mm after topical pilocarpine instillation showed 100% sensitivity and 82.8% specificity for detecting Adie’s tonic pupil. This study confirmed that pupillary constriction with 0.0625% pilocarpine is better than 0.125% pilocarpine for detecting denervation supersensitivity in Adie’s tonic pupil. Digital pupillometry is a reliable method for assessing denervation supersensitivity in Adie's tonic pupil.
Sivashakthi Kanagalingam,1–3 Neil R Miller1–31Department of Ophthalmology, 2Department of Neurology, 3Department of Neurosurgery, The Johns Hopkins Hospital, Baltimore, MD, USAAbstract: Horner syndrome consists of unilateral ptosis, an ipsilateral miotic but normally reactive pupil, and in some cases, ipsilateral facial anhidrosis, all resulting from damage to the ipsilateral oculosympathetic pathway. Herein, we review the clinical signs and symptoms that can aid in the diagnosis and localization of a Horner syndrome as well as the causes of the condition. We emphasize that pharmacologic testing can confirm its presence and direct further testing and management.Keywords: Horner syndrome, oculosympathoparesis, anisocoria, ptosis, anhidrosis
Horner syndrome is an uncommon but important clinical entity, representing interruption of the sympathetic pathway to the eye and face. Horner syndrome is almost always diagnosed clinically, though pharmacological testing can be used to confirm the diagnosis. Imaging modalities such as PET, CT and MRI are important components of work-up for patients presenting with acquired Horner syndrome. Our patient’s presentation with Horner syndrome unmasked the causative superior sulcus squamous cell carcinoma and a coincidental lower lobe adenocarcinoma. Successful radical treatment of these cancers resulted in complete resolution of the syndrome and disease-free survival at 18 months. We review the anatomy and pathophysiology underlying this and other causes of Horner syndrome.
Backgrounds:
Horner syndrome presents with ipsilateral ptosis, miosis, and anhidrosis due to interruption of the oculosympathetic pathway. Patients with acute ischemic stroke may present with Horner syndrome, which may help locate the lesion. However, the underlying pathways involved in Horner syndrome caused by isolated lenticulostriate ischemic stroke remain unclear.
Methods:
We screened consecutive patients with acute ischemic stroke admitted to the Second Affiliated Hospital of Guangzhou Medical University from 1 January 2020 to 31 December 2021, and searched for cases of isolated lenticulostriate strokes presenting with Horner syndrome. Strokes involving the brainstem or hypothalamus, or those caused by carotid dissection or carotid cavernous fistula were excluded based on neuroimaging and cerebrovascular examination.
Results:
Among the 1706 acute stroke patients, three patients developed temporary or long-term Horner syndrome due to an ipsilateral lenticulostriate ischemic lesion. Diffusion-tensor imaging revealed disruption of an uncrossed pathway from Brodmann areas 3, 1, and 2 through the basal ganglia to the ipsilateral hypothalamus.
Conclusion:
These findings suggest that Horner syndrome may be due to a disruption of an uncrossed cortico-basal ganglia-hypothalamic sympathetic pathway.
Horner syndrome results from an interruption of the oculosympathetic pathway. Patients with Horner syndrome present with a slightly droopy upper lid and a smaller pupil on the affected side; less commonly, there is a deficiency of sweating over the brow or face on the affected side. This condition does not usually cause vision problems or other significant symptoms, but is important as a warning sign that the oculosympathetic pathway has been interrupted, potentially with serious and even life-threatening processes. The oculosympathetic pathway has a long and circuitous course, beginning in the brain and traveling down the spinal cord to exit in the chest, then up the neck and into the orbit. Therefore, this syndrome with unimpressive clinical findings and insignificant symptoms may be a sign of serious pathology in the head, chest, or neck. This clinical review discusses how to identify the signs, confirm the diagnosis, and evaluate the many causes of Horner syndrome.
Purpose of review:
Anisocoria is a finding seen on a daily basis in nearly every eye clinic. Although often benign, it can also represent the sole sign of a life-threatening disease making an up-to-date understanding of pathophysiology and diagnosis essential for anyone practicing medicine.
Recent findings:
Many aspects of the traditional approach to anisocoria still hold true today, but advancements in imaging technology and changing trends in pharmacologic diagnosis and localization have led many to rethink that approach. In addition, the differential diagnosis for anisocoria continuously expands with identification and improved understanding of causal disease processes.
Summary:
The present article discusses an approach to the classic anisocoria diagnostic algorithm modified by current knowledge from the most recent literature.
Horner syndrome is typically described by the classic triad of blepharoptosis, miosis, and anhydrosis resulting from disruption along the oculosympathetic pathway. Because of the complex and extensive course of this pathway, there are a large number of causes of Horner syndrome ranging from benign to life-threatening diseases. This review article aims to provide a practical approach to investigation and management, including evaluation of the more recent use of apraclonidine for pharmacological testing.
The autonomic nervous system influences numerous ocular functions. It does this by way of parasympathetic innervation from postganglionic fibers that originate from neurons in the ciliary and pterygopalatine ganglia, and by way of sympathetic innervation from postganglionic fibers that originate from neurons in the superior cervical ganglion. Ciliary ganglion neurons project to the ciliary body and the sphincter pupillae muscle of the iris to control ocular accommodation and pupil constriction, respectively. Superior cervical ganglion neurons project to the dilator pupillae muscle of the iris to control pupil dilation. Ocular blood flow is controlled both via direct autonomic influences on the vasculature of the optic nerve, choroid, ciliary body, and iris, as well as via indirect influences on retinal blood flow. In mammals, this vasculature is innervated by vasodilatory fibers from the pterygopalatine ganglion, and by vasoconstrictive fibers from the superior cervical ganglion. Intraocular pressure is regulated primarily through the balance of aqueous humor formation and outflow. Autonomic regulation of ciliary body blood vessels and the ciliary epithelium is an important determinant of aqueous humor formation; autonomic regulation of the trabecular meshwork and episcleral blood vessels is an important determinant of aqueous humor outflow. These tissues are all innervated by fibers from the pterygopalatine and superior cervical ganglia. In addition to these classical autonomic pathways, trigeminal sensory fibers exert local, intrinsic influences on many of these regions of the eye, as well as on some neurons within the ciliary and pterygopalatine ganglia. © 2015 American Physiological Society. Compr Physiol 5: 439-473, 2015.
The aim of this study was to investigate the development of ideas about the nature and mechanism of the fixed dilated pupil, paying particular attention to experimental conditions and clinical observations in the 19th century. Starting from Kocher's standard review in 1901, the authors studied German, English, and French texts for historical information. Medical and neurological textbooks from the 19th and 20th centuries were reviewed to investigate when and how this information percolated through neurological and neurosurgical practices. Cooper experimented with intracranial pressure (ICP) in a dog in the 1830s, but did not mention the pupils. He described dilated pupils in clinical cases without referring to the effect of light. Bright demonstrated to have some knowledge of the pupil sign (clinical observations). Realizing the unreliability of the pupil sign, Hutchinson in 1867-1868 tried to reason in which cases trepanation would be advisable. Von Leyden's 1866 animal experiments, in which he increased CSF volume by injecting protein solutions intracranially, was the first observation in which the association between fixed dilated pupils and increased ICP was established. Along with bradycardia and motor and respiratory effects, he noticed wide pupils were usually present in a comatose state. Asymmetrical dilation could not always be attributed to increased ICP, but to an oculomotor nerve lesion. Pagenstecher in 1871 extended knowledge by meticulously studying consecutive pupil phenomena with increasing pressure. In 1880, von Bergmann emphasized the significance of the ipsilateral dilation in experiments as well as in clinical cases. He distinguished the extent of pressure increase and its duration. Probably confusing irritation (epileptic head turning to the other side with pupil dilation) and lesion effects, he suggested a cortical area responsible for oculomotor phenomena, indicating what is now known as the frontal eye field. Naunyn and Schreiber (1881) understood the relationship between increased ICP with pupil dilation and decreased pulse frequency and blood pressure, warning not to decrease the latter. Concentrating on experimental traumatic effects, Duret (1878) investigated compression and commotion, in which he distinguished two phases, notably pupil constriction by bulbar lesions, due to CSF shock, followed by dilation from congestion and inflammation, due to blood around the oculomotor nerve. The key observation of a fixed dilated pupil as a sign of acute mass effect came gradually and after some localization stumbles. Following the period of extensive experimental research in ICP, the results of which were translated to clinical observations, the prognostic significance was gradually acknowledged by authors of neurological textbooks. It is well known that Cushing did similar experiments in Berne (1900-1901), and later suggested he would not have done so if he had studied the literature.
Dilated pupil is a diagnostic challenge encountered by neurologists and ophthalmologists. The aim of this review is to provide an overview of the current data and guidelines concerning dilated pupils.
The majority of recent reports on dilated pupils are indicative of several medical conditions that require evaluation. The topical synthetic parasympatholytic agents; local contamination of antihistamines with their antimuscarinic effects; atropine, scopolamine, and tropane alkaloids in all species of Datura plants may produce mydriasis.
The causes of pupillary dilatation can be unilateral, bilateral, and transient. The clinical approach to dilated pupils requires stepwise evaluation, and based on the findings, unnecessary and costly procedures can be avoided.
First described in 1727, Horner syndrome occurs from injury to one of the three neurons in the oculo-sympathetic pathway. Its presence can be confirmed with pharmacologic testing, traditionally including cocaine testing with hydroxyamphetamine localization. More recently, apraclonidine testing has become a viable alternative in some practices. Concern has been raised regarding the possibility of false-negative results with apraclonidine testing as well as the safety of its use in young children.
Anisocoria, or a difference in pupil size, is a common condition. Its aetiology ranges from benign to life-threatening conditions. The clinical evaluation of anisocoria is discussed, emphasising the pharmacological aids (e.g., cocaine 10% eye drops, hydroxyamphetamine eye drops, pilocarpine 0.1% eye drops, pilocarpine 1% eye drops, apraclonidine) used in differentiating the different causes of anisocoria (e.g., physiological anisocoria, Horner syndrome, Adie pupil, pharmacological anisocoria, third nerve palsy).
Rendón Fernández H, Arias Del Peso B. Pupila tónica de Adie y otros signos asociados