Unequal pupil size, which may represent a benign physiologic variant or a manifestation of disease. Pathologic anisocoria reflects an abnormality in the musculature of the iris (IRIS DISEASES) or in the parasympathetic or sympathetic pathways that innervate the pupil. Physiologic anisocoria refers to an asymmetry of pupil diameter, usually less than 2mm, that is not associated with disease.
Constriction of the pupil in response to light stimulation of the retina. It refers also to any reflex involving the iris, with resultant alteration of the diameter of the pupil. (Cline et al., Dictionary of Visual Science, 4th ed)
The aperture in the iris through which light passes.
A syndrome characterized by a TONIC PUPIL that occurs in combination with decreased lower extremity reflexes. The affected pupil will respond more briskly to accommodation than to light (light-near dissociation) and is supersensitive to dilute pilocarpine eye drops, which induce pupillary constriction. Pathologic features include degeneration of the ciliary ganglion and postganglionic parasympathetic fibers that innervate the pupillary constrictor muscle. (From Adams et al., Principles of Neurology, 6th ed, p279)
Diseases of the oculomotor nerve or nucleus that result in weakness or paralysis of the superior rectus, inferior rectus, medial rectus, inferior oblique, or levator palpebrae muscles, or impaired parasympathetic innervation to the pupil. With a complete oculomotor palsy, the eyelid will be paralyzed, the eye will be in an abducted and inferior position, and the pupil will be markedly dilated. Commonly associated conditions include neoplasms, CRANIOCEREBRAL TRAUMA, ischemia (especially in association with DIABETES MELLITUS), and aneurysmal compression. (From Adams et al., Principles of Neurology, 6th ed, p270)
A syndrome associated with defective sympathetic innervation to one side of the face, including the eye. Clinical features include MIOSIS; mild BLEPHAROPTOSIS; and hemifacial ANHIDROSIS (decreased sweating)(see HYPOHIDROSIS). Lesions of the BRAIN STEM; cervical SPINAL CORD; first thoracic nerve root; apex of the LUNG; CAROTID ARTERY; CAVERNOUS SINUS; and apex of the ORBIT may cause this condition. (From Miller et al., Clinical Neuro-Ophthalmology, 4th ed, pp500-11)
The most anterior portion of the uveal layer, separating the anterior chamber from the posterior. It consists of two layers - the stroma and the pigmented epithelium. Color of the iris depends on the amount of melanin in the stroma on reflection from the pigmented epithelium.
Paralysis of one or more of the ocular muscles due to disorders of the eye muscles, neuromuscular junction, supporting soft tissue, tendons, or innervation to the muscles.
Adjustment of the eyes under conditions of low light. The sensitivity of the eye to light is increased during dark adaptation.

Waardenburg syndrome with anisocoria and exotropia. (1/20)

A case of Waardenburg syndrome with unusual features such as anisocoria, exotropia is reported.  (+info)

Proximal M2 false aneurysm after head trauma--Case report. (2/20)

A 72-year-old male presented with a post-traumatic false aneurysm of the right proximal M2 artery with massive subarachnoid hemorrhage after closed head injury. Serial computed tomography (CT) and angiography showed the development of the aneurysm which was verified at autopsy. He was admitted in a drowsy state just after a motorcycle accident. Initial brain CT showed subarachnoid hemorrhage without skull fracture. Follow-up brain CT showed a huge hematoma in the right temporal lobe. He died 47 hours after the accident. Histological examination of the aneurysm showed a false aneurysm. Delayed diagnosis of traumatic aneurysms leads to high mortality, so early surgical treatment is essential to save such patients.  (+info)

Late detection of supraclinoid carotid artery aneurysm after traumatic subarachnoid hemorrhage and occlusion of the ipsilateral cervical internal carotid artery. (3/20)

BACKGROUND AND PURPOSE: We report the first case of traumatic aneurysm of the supraclinoid internal carotid artery (ICA), which we speculate may have developed or grown after traumatic occlusion of the ipsilateral cervical ICA. CASE DESCRIPTION: A 26-year-old man presented with severe traumatic subarachnoid hemorrhage (SAH) and occlusion of the right cervical ICA after a motor vehicle accident. Three-dimensional CT angiography on admission showed no aneurysm. However, cerebral angiography 3 weeks after the injury showed a large aneurysm of the right supraclinoid ICA. The aneurysm was trapped, and pathological examination showed that it was a traumatic aneurysm. CONCLUSIONS: In this case we cannot be sure that the aneurysm was not present on admission. In view of the significant SAH, a lesson of this case may be to suspect such an aneurysm early on and perform early diagnostic cerebral angiography.  (+info)

Pupillary evaluation for differential diagnosis of coma. (4/20)

OBJECTIVES: To determine the usefulness of bedside evaluation of pupils in determining the aetiology of coma by adopting a probabilistic approach. PATIENTS AND METHODS: One hundred and fifteen consecutive patients presenting with coma were enrolled in this prospective cohort during the 12 month study period in the emergency room of a community teaching hospital. Patients underwent structured clinical examinations and laboratory and imaging tests. Assignment of aetiology of coma was based on strict adherence to predetermined criteria and achieved by consensus of the two physician investigators. One year follow up was obtained in all patients. RESULTS: Aetiology of coma was determined in 98% of the patients. It was metabolic in 69 patients (60%) and structural in 46 patients (40%). Metabolic causes included drug overdose, acute alcohol intoxication, hypoglycaemia, sepsis, and pneumonia. Structural causes included intracerebral haemorrhage, subarachnoid haemorrhage, cerebral infarction, subdural haematoma, and epidural haematoma. Multivariate logistic regression analysis showed light reflex loss (likelihood ratio for positive test result 3.59) and anisocoria (likelihood ratio for positive test result 9.0) as independent predictors of structural origin. CONCLUSIONS: In this prospective study of patients presenting to the emergency room of a community based teaching hospital with coma, in about 60% the coma is of metabolic origins and in about 40% of structural origins. Light reflex loss and anisocoria suggest a structural aetiology.  (+info)

The sensitivity and specificity of 0.5% apraclonidine in the diagnosis of oculosympathetic paresis. (5/20)

AIMS: To evaluate the sensitivity and specificity of 0.5% apraclonidine test in the diagnosis of oculosympathetic paresis (OSP). METHOD: Apraclonidine (0.5%) was administered to 31 eyes, nine with a diagnosis of Horner syndrome (HS), 22 with bilateral OSP caused by diabetes, and to 54 control eyes. All were confirmed with the cocaine test. The effects on pupil diameter and upper eyelid level were observed 1 hour later. RESULTS: Apraclonidine caused a mean dilation of 2.04 mm (range 1--4.5) (p<0.001) in the pupils with OSP and it caused pupillary constriction in the control eyes with a mean change of -0.14 mm (range 0.5 to --1) (p<0.05). It caused reversal of anisocoria in all HS cases. Its effects on both pupil diameters and upper lid levels differed significantly between the groups (p<0.001). The mean elevation in the upper lid was 1.75 mm (range 1--4) in the OSP group (p<0.001) and 0.61 mm (range 0--3) in the control group (p<0.001). CONCLUSION: The effect of the apraclonidine (0.5%) test on the pupil diameter was diagnostic for OSP and had at least the same sensitivity and specificity as the cocaine test for the diagnosis of OSP.  (+info)

When cluster headache was called histaminic cephalalgia (Horton's headache). (6/20)

The Author revives his experiences and reminiscences in the frontline research and everyday clinical practice dealing with what was then called "histaminic cephalalgia" (Horton's headache). In this context, the Author, one of the historical representatives of the School of Florence, reports an outline of the contribution of this pioneering period in order to promote research ideas concerning possible brain involvement in cluster headache (CH) pathogenesis, which is currently accepted worldwide. The recent history of CH has registered remarkable progress in revealing the mystery of this pathology and it is likely that, in the near future, through the development of better education and new treatments, the overall suffering of patients will be further minimised.  (+info)

Bilateral tonic pupils: Holmes Adie syndrome or generalised neuropathy? (7/20)

AIM: To compare the pupil signs in patients with bilateral pupillotonia caused by Holmes-Adie syndrome or generalised peripheral neuropathy. METHODS: Infrared video pupillographic techniques were used to measure a number of pupil variables in patients with Holmes-Adie syndrome, generalised neuropathy (various aetiologies) and healthy age-matched control subjects. RESULTS: Regardless of aetiology, the patients generally had pupil signs typical of pupillotonia (small dark diameters, large light diameters, tonic near responses, attenuated light responses with light-near dissociation, and sector palsy). However, significant differences were found in the prevalence and magnitude of several pupil variables in the two patient groups. In particular, sector palsy and anisocoria exceeding 1 mm (in the light) were seen much more commonly in Holmes-Adie patients than patients with generalised neuropathy. The presence of both these pupil signs can be used to distinguish between these diagnoses with a sensitivity of 58% and a specificity of 90%. CONCLUSIONS: The tonic pupils of patients with Holmes-Adie syndrome are significantly different to those found in patients with generalised neuropathy; recognition of these differences may allow distinction between these diagnoses.  (+info)

Sex-specific lateralization of contraction anisocoria in transient pupillary light reflex. (8/20)

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Anisocoria is a medical term that refers to an inequality in the size of the pupils in each eye. The pupil is the black, circular opening in the center of the iris (the colored part of the eye) that allows light to enter and strike the retina. Normally, the pupils are equal in size and react similarly when exposed to light or darkness. However, in anisocoria, one pupil is larger or smaller than the other.

Anisocoria can be caused by various factors, including neurological conditions, trauma, eye diseases, or medications that affect the pupillary reflex. In some cases, anisocoria may be a normal variant and not indicative of any underlying medical condition. However, if it is a new finding or associated with other symptoms such as pain, headache, vision changes, or decreased level of consciousness, it should be evaluated by a healthcare professional to determine the cause and appropriate treatment.

A pupillary reflex is a type of reflex that involves the constriction or dilation of the pupils in response to changes in light or near vision. It is mediated by the optic and oculomotor nerves. The pupillary reflex helps regulate the amount of light that enters the eye, improving visual acuity and protecting the retina from excessive light exposure.

In a clinical setting, the pupillary reflex is often assessed as part of a neurological examination. A normal pupillary reflex consists of both direct and consensual responses. The direct response occurs when light is shone into one eye and the pupil of that same eye constricts. The consensual response occurs when light is shone into one eye, causing the pupil of the other eye to also constrict.

Abnormalities in the pupillary reflex can indicate various neurological conditions, such as brainstem injuries or diseases affecting the optic or oculomotor nerves.

A pupil, in medical terms, refers to the circular opening in the center of the iris (the colored part of the eye) that allows light to enter and reach the retina. The size of the pupil can change involuntarily in response to light intensity and emotional state, as well as voluntarily through certain eye exercises or with the use of eye drops. Pupillary reactions are important in clinical examinations as they can provide valuable information about the nervous system's functioning, particularly the brainstem and cranial nerves II and III.

Adie syndrome, also known as Adie's pupil or tonic pupil, is a neurological disorder that affects the autonomic nervous system and the eye. It is characterized by a pupil that is dilated and unresponsive to light, but slowly constricts when focusing on nearby objects (a phenomenon called "light-near dissociation"). This occurs due to damage to the ciliary ganglion or the short ciliary nerves, which control the size of the pupil.

Additional symptoms of Adie syndrome may include decreased deep tendon reflexes, especially in the ankles, and abnormal sweating patterns. The condition is usually not painful and does not typically affect vision, although some people with Adie syndrome may experience difficulty with reading due to the slow pupillary response.

The exact cause of Adie syndrome is unknown, but it is thought to be related to a viral infection or an autoimmune disorder. It is more common in women than men and typically occurs between the ages of 20 and 40. While there is no cure for Adie syndrome, treatment may include the use of glasses with bifocal lenses or reading glasses, as well as physical therapy to improve muscle tone and reflexes.

The oculomotor nerve, also known as the third cranial nerve (CN III), is responsible for controlling several important eye movements and functions. Oculomotor nerve diseases refer to conditions that affect this nerve and can lead to various symptoms related to eye movement and function. Here's a medical definition of oculomotor nerve diseases:

Oculomotor nerve diseases are a group of medical disorders characterized by the dysfunction or damage to the oculomotor nerve (CN III), resulting in impaired eye movements, abnormalities in pupillary response, and potential effects on eyelid position. These conditions can be congenital, acquired, or traumatic in nature and may lead to partial or complete paralysis of the nerve. Common oculomotor nerve diseases include oculomotor nerve palsy, third nerve ganglionopathies, and compressive oculomotor neuropathies caused by various pathologies such as aneurysms, tumors, or infections.

Horner syndrome, also known as Horner's syndrome or oculosympathetic palsy, is a neurological disorder characterized by the interruption of sympathetic nerve pathways that innervate the head and neck, leading to a constellation of signs affecting the eye and face on one side of the body.

The classic triad of symptoms includes:

1. Ptosis (drooping) of the upper eyelid: This is due to the weakness or paralysis of the levator palpebrae superioris muscle, which is responsible for elevating the eyelid.
2. Miosis (pupillary constriction): The affected pupil becomes smaller in size compared to the other side, and it may not react as robustly to light.
3. Anhydrosis (decreased sweating): There is reduced or absent sweating on the ipsilateral (same side) of the face, particularly around the forehead and upper eyelid.

Horner syndrome can be caused by various underlying conditions, such as brainstem stroke, tumors, trauma, or certain medical disorders affecting the sympathetic nervous system. The diagnosis typically involves a thorough clinical examination, pharmacological testing, and sometimes imaging studies to identify the underlying cause. Treatment is directed towards managing the underlying condition responsible for Horner syndrome.

In medical terms, the iris refers to the colored portion of the eye that surrounds the pupil. It is a circular structure composed of thin, contractile muscle fibers (radial and circumferential) arranged in a regular pattern. These muscles are controlled by the autonomic nervous system and can adjust the size of the pupil in response to changes in light intensity or emotional arousal. By constricting or dilating the iris, the amount of light entering the eye can be regulated, which helps maintain optimal visual acuity under various lighting conditions.

The color of the iris is determined by the concentration and distribution of melanin pigments within the iris stroma. The iris also contains blood vessels, nerves, and connective tissue that support its structure and function. Anatomically, the iris is continuous with the ciliary body and the choroid, forming part of the uveal tract in the eye.

Ophthalmoplegia is a medical term that refers to the paralysis or weakness of the eye muscles, which can result in double vision (diplopia) or difficulty moving the eyes. It can be caused by various conditions, including nerve damage, muscle disorders, or neurological diseases such as myasthenia gravis or multiple sclerosis. Ophthalmoplegia can affect one or more eye muscles and can be partial or complete. Depending on the underlying cause, ophthalmoplegia may be treatable with medications, surgery, or other interventions.

Dark adaptation is the process by which the eyes adjust to low levels of light. This process allows the eyes to become more sensitive to light and see better in the dark. It involves the dilation of the pupils, as well as chemical changes in the rods and cones (photoreceptor cells) of the retina. These changes allow the eye to detect even small amounts of light and improve visual acuity in low-light conditions. Dark adaptation typically takes several minutes to occur fully, but can be faster or slower depending on various factors such as age, prior exposure to light, and certain medical conditions. It is an important process for maintaining good vision in a variety of lighting conditions.

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