Iridoplegia

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Iridoplegia is the paralysis of the sphincter of the iris. It can occur in due to direct orbital injury, which may result in short lived blurred vision. [1]

Contents

Types

It can be of three types:

  1. accommodative iridoplegia- Noncontraction of pupils during accommodation.
  2. complete iridoplegia- Iris fails to respond to any stimulation.
  3. reflex iridoplegia- The absence of light reflex, with retention of accommodation reflex. Also called Argyll Robertson pupil.

Etiology

Iridoplegia has been reported in association with Guillain-Barré syndrome. [2]

Related Research Articles

Pupil part of an eye

The pupil is a black hole located in the center of the iris of the eye that allows light to strike the retina. It appears black because light rays entering the pupil are either absorbed by the tissues inside the eye directly, or absorbed after diffuse reflections within the eye that mostly miss exiting the narrow pupil. The term “pupil” was created by Gerard of Cremona.

Optic nerve paired nerve that transmits visual information from the retina to the brain

The optic nerve, also known as cranial nerve II, or simply as CN II, is a paired cranial nerve that transmits visual information from the retina to the brain. In humans, the optic nerve is derived from optic stalks during the seventh week of development and is composed of retinal ganglion cell axons and glial cells; it extends from the optic disc to the optic chiasma and continues as the optic tract to the lateral geniculate nucleus, pretectal nuclei, and superior colliculus.

Mydriasis Excessive dilation of the pupil

Mydriasis is the dilation of the pupil, usually having a non-physiological cause, or sometimes a physiological pupillary response. Non-physiological causes of mydriasis include disease, trauma, or the use of drugs.

Pupillary light reflex reflex controlling the diameter of the pupil in response to the intensity of light

The pupillary light reflex (PLR) or photopupillary reflex is a reflex that controls the diameter of the pupil, in response to the intensity (luminance) of light that falls on the retinal ganglion cells of the retina in the back of the eye, thereby assisting in adaptation of vision to various levels of lightness/darkness. A greater intensity of light causes the pupil to constrict, whereas a lower intensity of light causes the pupil to dilate. Thus, the pupillary light reflex regulates the intensity of light entering the eye. Light shone into one eye will cause both pupils to constrict.

Human eye Mammalian eye; part of the visual organ of the human body, and move using a system of six muscles

The human eye is an organ that reacts to light and allows vision. Rod and cone cells in the retina allow conscious light perception and vision including color differentiation and the perception of depth. The human eye can differentiate between about 10 million colors and is possibly capable of detecting a single photon. The eye is part of the sensory nervous system.

Horners syndrome Human disease characterized by miosis (a constricted pupil), partial ptosis (a weak, droopy eyelid), apparent anhydrosis (decreased sweating), with apparent enophthalmos (inset eyeball)

Horner's syndrome, also known as oculosympathetic paresis, is a combination of symptoms that arises when a group of nerves known as the sympathetic trunk is damaged. The signs and symptoms occur on the same side (ipsilateral) as it is a lesion of the sympathetic trunk. It is characterized by miosis, partial ptosis, apparent anhydrosis, with apparent enophthalmos.

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Ciliary ganglion parasympathetic ganglion located just behind the eye in the posterior orbit

The ciliary ganglion is a bundle of nerve parasympathetic ganglion located just behind the eye in the posterior orbit. It is 1–2 mm in diameter and in humans contains approximately 2,500 neurons. The ganglion contains postganglionic parasympathetic neurons. These neurons supply the pupillary sphincter muscle, which constricts the pupil, and the ciliary muscle which contracts to make the lens more convex. Both of these muscles are involuntary since they are controlled by the parasympathetic division of the autonomic nervous system.

Adie syndrome neurological disorder characterized by a tonically dilated pupil

Adie syndrome, also known as Holmes-Adie syndrome, is a neurological disorder characterized by a tonically dilated pupil that reacts slowly to light but shows a more definite response to accommodation. It is frequently seen in females with absent knee or ankle jerks and impaired sweating.

Anisocoria condition characterized by an unequal size of the eyes pupils

Anisocoria is a condition characterized by an unequal size of the eyes' pupils. Affecting up to 20% of the population, anisocoria is often entirely harmless, but can be a sign of more serious medical problems.

Hyporeflexia refers to below normal or absent reflexes (areflexia). It can be detected through the use of a reflex hammer. It is the opposite of hyperreflexia. Hyporeflexia is generally associated with a lower motor neuron deficit, whereas hyperreflexia is often attributed to upper motor neuron lesions. The upper motor neurons are thought to inhibit the reflex arc, which is formed by sensory neurons from intrafusal fibers of muscles, lower motor neurons and appurtenant interneurons. Therefore, damage to lower motor neurons will subsequently result in hyporeflexia and/or areflexia.

GM1 Biochemical compound important in the brain and intestines

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André Strohl French physician

André Strohl was a French physiologist who was a native of Poitiers. He is remembered for his role in the diagnosis of Guillain–Barré syndrome, a form of areflexic paralysis which exhibits normal cell count but with an abnormal increase in spinal fluid protein. The syndrome is named after two French neurologists; Georges Guillain and Jean Alexandre Barré.

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Lower motor neuron lesion

A lower motor neuron lesion is a lesion which affects nerve fibers traveling from the lower motor neuron(s) in the anterior horn/anterior grey column of the spinal cord, or in the motor nuclei of the cranial nerves, to the relevant muscle(s).

Guillain–Barré syndrome (GBS) is a rapid-onset muscle weakness caused by the immune system damaging the peripheral nervous system. The initial symptoms are typically changes in sensation or pain along with muscle weakness, beginning in the feet and hands, often spreading to the arms and upper body, with both sides being involved. The symptoms may develop over hours to a few weeks. During the acute phase, the disorder can be life-threatening, with about 15 percent of people developing weakness of the breathing muscles and, therefore, requiring mechanical ventilation. Some are affected by changes in the function of the autonomic nervous system, which can lead to dangerous abnormalities in heart rate and blood pressure.

Acute motor axonal neuropathy (AMAN) is a variant of Guillain–Barré syndrome. It is characterized by acute paralysis and loss of reflexes without sensory loss. Pathologically, there is motor axonal degeneration with antibody-mediated attacks of motor nerves and nodes of Ranvier.

Antiganglioside antibodies that react to self-gangliosides are found in autoimmune neuropathies. These antibodies were first found to react with cerebellar cells. These antibodies show highest association with certain forms of Guillain–Barré syndrome.

Bickerstaff brainstem encephalitis is a rare inflammatory disorder of the central nervous system, first described by Edwin Bickerstaff in 1951. It may also affect the peripheral nervous system, and has features in common with both Miller Fisher syndrome and Guillain–Barré syndrome.

Accommodative excess

In ophthalmology, accommodative excess occurs when an individual uses more than normal accommodation for performing certain near work. Accommodative excess has traditionally been defined as accommodation that is persistently higher than expected for the patient's age. Modern definitions simply regard it as an inability to relax accommodation readily. Excessive accommodation is seen in association with excessive convergence also.

References

  1. Harrison's neurology in clinical medicine. Harrison, Tinsley Randolph, 1900-1978., Hauser, Stephen L., Josephson, Scott Andrew. (2nd ed.). New York: McGraw-Hill Medical. 2010. p. 402. ISBN   9780071741033. OCLC   477051832.CS1 maint: others (link)
  2. HUNG, J. C C; APPLETON, R. E (1 July 1997). "Iridoplegia in severe Guillain-Barre syndrome". Archives of Disease in Childhood. 77 (1): 91–91. doi:10.1136/adc.77.1.91a. PMC   1717230 . PMID   9279166.