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.
A mitochondrial myopathy characterized by slowly progressive paralysis of the levator palpebrae, orbicularis oculi, and extraocular muscles. Ragged-red fibers and atrophy are found on muscle biopsy. Familial and sporadic forms may occur. Disease onset is usually in the first or second decade of life, and the illness slowly progresses until usually all ocular motility is lost. (From Adams et al., Principles of Neurology, 6th ed, p1422)
A mitochondrial disorder featuring the triad of chronic progressive EXTERNAL OPHTHALMOPLEGIA, cardiomyopathy (CARDIOMYOPATHIES) with conduction block (HEART BLOCK), and RETINITIS PIGMENTOSA. Disease onset is in the first or second decade. Elevated CSF protein, sensorineural deafness, seizures, and pyramidal signs may also be present. Ragged-red fibers are found on muscle biopsy. (Adams et al., Principles of Neurology, 6th ed, p984)
A variant of the GUILLAIN-BARRE SYNDROME characterized by the acute onset of oculomotor dysfunction, ataxia, and loss of deep tendon reflexes with relative sparing of strength in the extremities and trunk. The ataxia is produced by peripheral sensory nerve dysfunction and not by cerebellar injury. Facial weakness and sensory loss may also occur. The process is mediated by autoantibodies directed against a component of myelin found in peripheral nerves. (Adams et al., Principles of Neurology, 6th ed, p1313; Neurology 1987 Sep;37(9):1493-8)
Drooping of the upper lid due to deficient development or paralysis of the levator palpebrae muscle.
Disorders that feature impairment of eye movements as a primary manifestation of disease. These conditions may be divided into infranuclear, nuclear, and supranuclear disorders. Diseases of the eye muscles or oculomotor cranial nerves (III, IV, and VI) are considered infranuclear. Nuclear disorders are caused by disease of the oculomotor, trochlear, or abducens nuclei in the BRAIN STEM. Supranuclear disorders are produced by dysfunction of higher order sensory and motor systems that control eye movements, including neural networks in the CEREBRAL CORTEX; BASAL GANGLIA; CEREBELLUM; and BRAIN STEM. Ocular torticollis refers to a head tilt that is caused by an ocular misalignment. Opsoclonus refers to rapid, conjugate oscillations of the eyes in multiple directions, which may occur as a parainfectious or paraneoplastic condition (e.g., OPSOCLONUS-MYOCLONUS SYNDROME). (Adams et al., Principles of Neurology, 6th ed, p240)
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.
Double-stranded DNA of MITOCHONDRIA. In eukaryotes, the mitochondrial GENOME is circular and codes for ribosomal RNAs, transfer RNAs, and about 10 proteins.
An irregularly shaped venous space in the dura mater at either side of the sphenoid bone.
Virus infection of the Gasserian ganglion and its nerve branches characterized by pain and vesicular eruptions with much swelling. Ocular involvement is usually heralded by a vesicle on the tip of the nose. This area is innervated by the nasociliary nerve.
Abnormal protrusion of both eyes; may be caused by endocrine gland malfunction, malignancy, injury, or paralysis of the extrinsic muscles of the eye.
The muscles that move the eye. Included in this group are the medial rectus, lateral rectus, superior rectus, inferior rectus, inferior oblique, superior oblique, musculus orbitalis, and levator palpebrae superioris.
An idiopathic syndrome characterized by the formation of granulation tissue in the anterior cavernous sinus or superior orbital fissure, producing a painful ophthalmoplegia. (Adams et al., Principles of Neurology, 6th ed, p271)
A visual symptom in which a single object is perceived by the visual cortex as two objects rather than one. Disorders associated with this condition include REFRACTIVE ERRORS; STRABISMUS; OCULOMOTOR NERVE DISEASES; TROCHLEAR NERVE DISEASES; ABDUCENS NERVE DISEASES; and diseases of the BRAIN STEM and OCCIPITAL LOBE.
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 group of muscle diseases associated with abnormal mitochondria function.
Diseases caused by abnormal function of the MITOCHONDRIA. They may be caused by mutations, acquired or inherited, in mitochondrial DNA or in nuclear genes that code for mitochondrial components. They may also be the result of acquired mitochondria dysfunction due to adverse effects of drugs, infections, or other environmental causes.
An acute neurological disorder characterized by the triad of ophthalmoplegia, ataxia, and disturbances of mental activity or consciousness. Eye movement abnormalities include nystagmus, external rectus palsies, and reduced conjugate gaze. THIAMINE DEFICIENCY and chronic ALCOHOLISM are associated conditions. Pathologic features include periventricular petechial hemorrhages and neuropil breakdown in the diencephalon and brainstem. Chronic thiamine deficiency may lead to KORSAKOFF SYNDROME. (Adams et al., Principles of Neurology, 6th ed, pp1139-42; Davis & Robertson, Textbook of Neuropathology, 2nd ed, pp452-3)
A heterogenous group of disorders characterized by alterations of mitochondrial metabolism that result in muscle and nervous system dysfunction. These are often multisystemic and vary considerably in age at onset (usually in the first or second decade of life), distribution of affected muscles, severity, and course. (From Adams et al., Principles of Neurology, 6th ed, pp984-5)
The 6th cranial nerve which originates in the ABDUCENS NUCLEUS of the PONS and sends motor fibers to the lateral rectus muscles of the EYE. Damage to the nerve or its nucleus disrupts horizontal eye movement control.
Diseases of the sixth cranial (abducens) nerve or its nucleus in the pons. The nerve may be injured along its course in the pons, intracranially as it travels along the base of the brain, in the cavernous sinus, or at the level of superior orbital fissure or orbit. Dysfunction of the nerve causes lateral rectus muscle weakness, resulting in horizontal diplopia that is maximal when the affected eye is abducted and ESOTROPIA. Common conditions associated with nerve injury include INTRACRANIAL HYPERTENSION; CRANIOCEREBRAL TRAUMA; ISCHEMIA; and INFRATENTORIAL NEOPLASMS.
A subtype of mitochondrial ADP, ATP translocase found primarily in heart muscle (MYOCARDIUM) and skeletal muscle (MUSCLE, SKELETAL).
Disorders of one or more of the twelve cranial nerves. With the exception of the optic and olfactory nerves, this includes disorders of the brain stem nuclei from which the cranial nerves originate or terminate.
Impairment of the ability to perform smoothly coordinated voluntary movements. This condition may affect the limbs, trunk, eyes, pharynx, larynx, and other structures. Ataxia may result from impaired sensory or motor function. Sensory ataxia may result from posterior column injury or PERIPHERAL NERVE DISEASES. Motor ataxia may be associated with CEREBELLAR DISEASES; CEREBRAL CORTEX diseases; THALAMIC DISEASES; BASAL GANGLIA DISEASES; injury to the RED NUCLEUS; and other conditions.
The 3d cranial nerve. The oculomotor nerve sends motor fibers to the levator muscles of the eyelid and to the superior rectus, inferior rectus, and inferior oblique muscles of the eye. It also sends parasympathetic efferents (via the ciliary ganglion) to the muscles controlling pupillary constriction and accommodation. The motor fibers originate in the oculomotor nuclei of the midbrain.
Involuntary movements of the eye that are divided into two types, jerk and pendular. Jerk nystagmus has a slow phase in one direction followed by a corrective fast phase in the opposite direction, and is usually caused by central or peripheral vestibular dysfunction. Pendular nystagmus features oscillations that are of equal velocity in both directions and this condition is often associated with visual loss early in life. (Adams et al., Principles of Neurology, 6th ed, p272)
Acquired, familial, and congenital disorders of SKELETAL MUSCLE and SMOOTH MUSCLE.
Neoplasms of the bony orbit and contents except the eyeball.
A rare central nervous system demyelinating condition affecting children and young adults. Pathologic findings include a large, sharply defined, asymmetric focus of myelin destruction that may involve an entire lobe or cerebral hemisphere. The clinical course tends to be progressive and includes dementia, cortical blindness, cortical deafness, spastic hemiplegia, and pseudobulbar palsy. Concentric sclerosis of Balo is differentiated from diffuse cerebral sclerosis of Schilder by the pathologic finding of alternating bands of destruction and preservation of myelin in concentric rings. Alpers' Syndrome refers to a heterogeneous group of diseases that feature progressive cerebral deterioration and liver disease. (From Adams et al., Principles of Neurology, 6th ed, p914; Dev Neurosci 1991;13(4-5):267-73)
A nonspecific tumor-like inflammatory lesion in the ORBIT of the eye. It is usually composed of mature LYMPHOCYTES; PLASMA CELLS; MACROPHAGES; LEUKOCYTES with varying degrees of FIBROSIS. Orbital pseudotumors are often associated with inflammation of the extraocular muscles (ORBITAL MYOSITIS) or inflammation of the lacrimal glands (DACRYOADENITIS).
Mitochondria of skeletal and smooth muscle. It does not include myocardial mitochondria for which MITOCHONDRIA, HEART is available.
A type of ILEUS, a functional not mechanical obstruction of the INTESTINES. This syndrome is caused by a large number of disorders involving the smooth muscles (MUSCLE, SMOOTH) or the NERVOUS SYSTEM.
Recording of the average amplitude of the resting potential arising between the cornea and the retina in light and dark adaptation as the eyes turn a standard distance to the right and the left. The increase in potential with light adaptation is used to evaluate the condition of the retinal pigment epithelium.
A general term encompassing lower MOTOR NEURON DISEASE; PERIPHERAL NERVOUS SYSTEM DISEASES; and certain MUSCULAR DISEASES. Manifestations include MUSCLE WEAKNESS; FASCICULATION; muscle ATROPHY; SPASM; MYOKYMIA; MUSCLE HYPERTONIA, myalgias, and MUSCLE HYPOTONIA.
Voluntary or reflex-controlled movements of the eye.
A subclass of ACIDIC GLYCOSPHINGOLIPIDS. They contain one or more sialic acid (N-ACETYLNEURAMINIC ACID) residues. Using the Svennerholm system of abbrevations, gangliosides are designated G for ganglioside, plus subscript M, D, or T for mono-, di-, or trisialo, respectively, the subscript letter being followed by a subscript arabic numeral to indicated sequence of migration in thin-layer chromatograms. (From Oxford Dictionary of Biochemistry and Molecular Biology, 1997)
Bony cavity that holds the eyeball and its associated tissues and appendages.
A characteristic symptom complex.
Severe or complete loss of facial muscle motor function. This condition may result from central or peripheral lesions. Damage to CNS motor pathways from the cerebral cortex to the facial nuclei in the pons leads to facial weakness that generally spares the forehead muscles. FACIAL NERVE DISEASES generally results in generalized hemifacial weakness. NEUROMUSCULAR JUNCTION DISEASES and MUSCULAR DISEASES may also cause facial paralysis or paresis.
The front part of the hindbrain (RHOMBENCEPHALON) that lies between the MEDULLA and the midbrain (MESENCEPHALON) ventral to the cerebellum. It is composed of two parts, the dorsal and the ventral. The pons serves as a relay station for neural pathways between the CEREBELLUM to the CEREBRUM.
Diseases of the fourth cranial (trochlear) nerve or its nucleus in the midbrain. The nerve crosses as it exits the midbrain dorsally and may be injured along its course through the intracranial space, cavernous sinus, superior orbital fissure, or orbit. Clinical manifestations include weakness of the superior oblique muscle which causes vertical DIPLOPIA that is maximal when the affected eye is adducted and directed inferiorly. Head tilt may be seen as a compensatory mechanism for diplopia and rotation of the visual axis. Common etiologies include CRANIOCEREBRAL TRAUMA and INFRATENTORIAL NEOPLASMS.
Inflammation of a transverse portion of the spinal cord characterized by acute or subacute segmental demyelination or necrosis. The condition may occur sporadically, follow an infection or vaccination, or present as a paraneoplastic syndrome (see also ENCEPHALOMYELITIS, ACUTE DISSEMINATED). Clinical manifestations include motor weakness, sensory loss, and incontinence. (Adams et al., Principles of Neurology, 6th ed, pp1242-6)
Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques.
DNA-dependent DNA polymerases found in bacteria, animal and plant cells. During the replication process, these enzymes catalyze the addition of deoxyribonucleotide residues to the end of a DNA strand in the presence of DNA as template-primer. They also possess exonuclease activity and therefore function in DNA repair.
Diseases of the bony orbit and contents except the eyeball.
An acute inflammatory autoimmune neuritis caused by T cell- mediated cellular immune response directed towards peripheral myelin. Demyelination occurs in peripheral nerves and nerve roots. The process is often preceded by a viral or bacterial infection, surgery, immunization, lymphoma, or exposure to toxins. Common clinical manifestations include progressive weakness, loss of sensation, and loss of deep tendon reflexes. Weakness of respiratory muscles and autonomic dysfunction may occur. (From Adams et al., Principles of Neurology, 6th ed, pp1312-1314)
Diseases affecting or involving the PARANASAL SINUSES and generally manifesting as inflammation, abscesses, cysts, or tumors.
Incoordination of voluntary movements that occur as a manifestation of CEREBELLAR DISEASES. Characteristic features include a tendency for limb movements to overshoot or undershoot a target (dysmetria), a tremor that occurs during attempted movements (intention TREMOR), impaired force and rhythm of diadochokinesis (rapidly alternating movements), and GAIT ATAXIA. (From Adams et al., Principles of Neurology, 6th ed, p90)
A glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states.
Death resulting from the presence of a disease in an individual, as shown by a single case report or a limited number of patients. This should be differentiated from DEATH, the physiological cessation of life and from MORTALITY, an epidemiological or statistical concept.
A disorder of neuromuscular transmission characterized by weakness of cranial and skeletal muscles. Autoantibodies directed against acetylcholine receptors damage the motor endplate portion of the NEUROMUSCULAR JUNCTION, impairing the transmission of impulses to skeletal muscles. Clinical manifestations may include diplopia, ptosis, and weakness of facial, bulbar, respiratory, and proximal limb muscles. The disease may remain limited to the ocular muscles. THYMOMA is commonly associated with this condition. (Adams et al., Principles of Neurology, 6th ed, p1459)

Absent pituitary gland and hypoplasia of the cerebellar vermis associated with partial ophthalmoplegia and postaxial polydactyly: a variant of orofaciodigital syndrome VI or a new syndrome? (1/328)

We report two sibs with features overlapping those of orofaciodigital syndrome type VI (Varadi syndrome). Both presented at birth with oculomotor abnormalities, dysmorphic facial features, and dysgenesis of the cerebellar vermis. There were minimal oral manifestations (high arched palate) in both of them and one had postaxial polydactyly of both hands and one foot. In addition, there was evidence of aplasia of the pituitary gland on MRI scan in both of them with evidence of hypopituitarism. Both responded well to hormone replacement therapy with improvement in their linear growth and mental ability. These cases may represent a new autosomal recessive midline defect syndrome with features overlapping OFDS VI. Alternatively the features in these children could represent variability within OFDS VI.  (+info)

Congenital myasthenia gravis: clinical and HLA studies in two brothers. (2/328)

Two brothers with congenital myasthenia gravis are described. In both, ptosis and ophthalmoplegia responded poorly to oral anticholinesterase therapy and to thymectomy. The brothers had two different HLA haplotypes and neither had the HLA-A1-B8-DW3 haplotypes which are commonly associated with myathenia gravis in adult-onset cases.  (+info)

Dominant hereditary inclusion-body myopathy gene (IBM3) maps to chromosome region 17p13.1. (3/328)

We recently described an autosomal dominant inclusion-body myopathy characterized by congenital joint contractures, external ophthalmoplegia, and predominantly proximal muscle weakness. A whole-genome scan, performed with 161 polymorphic markers and with DNA from 40 members of one family, indicated strong linkage for markers on chromosome 17p. After analyses with additional markers in the region and with DNA from eight additional family members, a maximum LOD score (Zmax) was detected for marker D17S1303 (Zmax=7.38; recombination fraction (theta)=0). Haplotype analyses showed that the locus (Genome Database locus name: IBM3) is flanked distally by marker D17S945 and proximally by marker D17S969. The positions of cytogenetically localized flanking markers suggest that the location of the IBM3 gene is in chromosome region 17p13.1. Radiation hybrid mapping showed that IBM3 is located in a 2-Mb chromosomal region and that the myosin heavy-chain (MHC) gene cluster, consisting of at least six genes, co-localizes to the same region. This localization raises the possibility that one of the MHC genes clustered in this region may be involved in this disorder.  (+info)

Tolosa Hunt syndrome: a case report. Clinical and magnetic resonance imaging findings. (4/328)

A 36-year-old woman was admitted with a left abducens nerve palsy. MR showed enlargement of the left cavernous sinus. The patient was treated with 80 mg oral methyl prednisolone. Clinical findings improved within a month. Two months later, she was readmitted with left oculomotor and right abducens nerve palsy. MR showed significant increase in the volume of the abnormal area in the left cavernous sinus and a new lesion within the right cavernous sinus. After intravenous gadolinium DTPA, there was enhancement in both cavernous sinuses. Methyl prednisolone therapy was again started. After one month of treatment neurological examination was normal. Follow-up MR findings were similar to previous ones.  (+info)

Clinical genetics of familial progressive supranuclear palsy. (5/328)

Recent studies have shown that progressive supranuclear palsy (PSP) could be inherited, but the pattern of inheritance and the spectrum of the clinical findings in relatives are unknown. We here report 12 pedigrees, confirmed by pathology in four probands, with familial PSP. Pathological diagnosis was confirmed according to recently reported internationally agreed criteria. The spectrum of the clinical phenotypes in these families was variable including 34 typical cases of PSP (12 probands plus 22 secondary cases), three patients with postural tremor, three with dementia, one with parkinsonism, two with tremor, dystonia, gaze palsy and tics, and one with gait disturbance. The presence of affected members in at least two generations in eight of the families and the absence of consanguinity suggests autosomal dominant transmission with incomplete penetrance. We conclude that hereditary PSP is more frequent than previously thought and that the scarcity of familial cases may be related to a lack of recognition of the variable phenotypic expression of the disease.  (+info)

CFEOM3: a new extraocular congenital fibrosis syndrome that maps to 16q24.2-q24.3. (6/328)

PURPOSE: To define the clinical characteristics and determine the gene localization for a previously undescribed form of congenital fibrosis of the extraocular muscles (CFEOM), referred to as CFEOM type 3 (CFEOM3). METHODS: A large family with CFEOM was identified, and participating individuals underwent ophthalmologic examination and donated blood for genetic analysis. The family's disorder was tested for linkage to the known CFEOM loci, followed by a genome-wide search and linkage refinement using polymorphic DNA markers. RESULTS: Thirty-eight members of this Canadian family participated in the study. Affected individuals are born with a nonprogressive eye movement disorder characterized by variable expression of ptosis and restrictive external ophthalmoplegia. Severely affected individuals have ptosis, primary gaze fixed in a hypo- and exotropic position, and marked restriction of eye movement bilaterally. Mildly affected individuals have normally positioned globes with a limitation of vertical gaze. Moderately affected individuals have asymmetrical involvement with one eye severely and one eye mildly affected. The disorder is autosomal dominant with variable expression and probable incomplete penetrance. Genetic analysis reveals linkage to markers on 16q24.2q24.3. A maximum lod score of 5.8 occurs at markers D16S3063 and D16S689, and the CFEOM3 disease gene is located within a 5.6-cM region flanked by D16S486 and D16S671. CONCLUSIONS: These data establish that CFEOM3 is a phenotypically variant and genotypically distinct form of CFEOM with linkage to chromosome 16qter. The authors have previously demonstrated that CFEOM1 results from a developmental absence of the superior division of the oculomotor nerve. The authors hypothesize that CFEOM3 results from a defect analogous to, but distinct from CFEOM1.  (+info)

Neuro-Behcet's disease presenting with isolated unilateral lateral rectus muscle palsy. (7/328)

The authors present the clinical findings of a 30-year-old female and a 29-year-old male who both had isolated unilateral lateral rectus muscle palsy in neuro-Behcet's disease. The clinical feature related to isolated abduscens nerve palsy was identified by CT, systemic assessment and extraocular examination. These patients' constellation of findings appear to be unique: it does not follow any previously reported pattern of ocular manifestations of neuro-Behcet's disease.  (+info)

Proprioceptive and retinal afference modify postsaccadic ocular drift. (8/328)

Drift of the eyes after saccades produces motion of images on the retina (retinal slip) that degrades visual acuity. In this study, we examined the contributions of proprioceptive and retinal afference to the suppression of postsaccadic drift induced by a unilateral ocular muscle paresis. Eye movements were recorded in three rhesus monkeys with a unilateral weakness of one vertical extraocular muscle before and after proprioceptive deafferentation of the paretic eye. Postsaccadic drift was examined in four visual states: monocular viewing with the normal eye (4-wk period); binocular viewing (2-wk period); binocular viewing with a disparity-reducing prism (2-wk period); and monocular viewing with the paretic eye (2-wk period). The muscle paresis produced vertical postsaccadic drift in the paretic eye, and this drift was suppressed in the binocular viewing condition even when the animals could not fuse. When the animals viewed binocularly with a disparity-reducing prism, the drift in the paretic eye was suppressed in two monkeys (with superior oblique pareses) but generally was enhanced in one animal (with a tenotomy of the inferior rectus). When drift movements were enhanced, they reduced the retinal disparity that was present at the end of the saccade. In the paretic-eye-viewing condition, postsaccadic drift was suppressed in the paretic eye and was induced in the normal eye. After deafferentation in the normal-eye-viewing state, there was a change in the vertical postsaccadic drift of the paretic eye. This change in drift was idiosyncratic and variably affected the amplitude and velocity of the postsaccadic drift movements of the paretic eye. Deafferentation of the paretic eye did not affect the postsaccadic drift of the normal eye nor did it impair visually mediated adaptation of postsaccadic drift. The results demonstrate several new findings concerning the roles of visual and proprioceptive afference in the control of postsaccadic drift: disconjugate adaptation of postsaccadic drift does not require binocular fusion; slow, postsaccadic drift movements that reduce retinal disparity but concurrently increase retinal slip can be induced in the binocular viewing state; postsaccadic drift is modified by proprioception from the extraocular muscles, but these modifications do not serve to minimize retinal slip or to correct errors in saccade amplitude; and visually mediated adaptation of postsaccadic drift does not require proprioceptive afference from the paretic eye.  (+info)

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.

Chronic Progressive External Ophthalmoplegia (CPEO) is a rare, progressive neuromuscular disorder that affects the extraocular muscles, which are responsible for eye movement. This results in progressive weakness and paralysis of these muscles, leading to limitations in eye movement and, subsequently, binocular vision.

The term "chronic" refers to the slow, gradual progression of symptoms over time, while "progressive" highlights the worsening nature of the condition. "External" indicates that the extraocular muscles are involved, as opposed to the "internal" ophthalmoplegia, which would refer to the paralysis of the iris and ciliary body muscles within the eye.

CPEO is characterized by symmetrical, bilateral paresis (partial paralysis) or complete paralysis of the extraocular muscles, leading to drooping eyelids (ptosis), limited eye movements in all directions, and double vision (diplopia). The onset of symptoms typically occurs during adulthood, but it can also manifest in childhood.

CPEO is often associated with mitochondrial DNA abnormalities or mutations, which can lead to impaired energy production within the cells. This specific type of ophthalmoplegia is generally not linked to other neurological or systemic symptoms, but it can co-occur with additional manifestations in some cases, forming a broader spectrum of mitochondrial disorders known as Kearns-Sayre syndrome (KSS) or oculocraniosomatic syndrome.

There is no cure for CPEO, and management primarily focuses on addressing the symptoms and improving quality of life. Treatment options may include surgical interventions to correct ptosis or strabismus (squint), as well as supportive care such as visual aids and rehabilitation strategies.

Kearns-Sayre Syndrome (KSS) is a rare, progressive genetic disorder that affects the function of the mitochondria, which are the energy-producing structures in cells. It is classified as a type of mitochondrial myopathy and is typically associated with symptoms that appear before the age of 20.

The medical definition of Kearns-Sayre Syndrome includes the following criteria:
1. Onset before 20 years of age
2. Progressive external ophthalmoplegia (PEO), which is characterized by weakness and paralysis of the eye muscles, leading to drooping eyelids (ptosis) and limited eye movement
3. Retinitis pigmentosa, a degenerative condition affecting the retina that can lead to vision loss
4. A cardiac conduction defect, such as heart block
5. Ragged red fibers on muscle biopsy
6. At least one major criteria or two minor criteria must be present:
* Major criteria include cerebellar ataxia (lack of coordination), deafness, or increased protein in the cerebrospinal fluid
* Minor criteria include pigmentary retinopathy, heart block, or a high level of creatine kinase in the blood.

Kearns-Sayre Syndrome is caused by a single large-scale deletion of genes in the mitochondrial DNA and is usually sporadic, meaning it occurs randomly and is not inherited from parents. The condition can be diagnosed through genetic testing, muscle biopsy, or other clinical tests. Treatment is focused on managing symptoms and may include physical therapy, surgery for ptosis, hearing aids, and pacemakers for heart block.

Miller Fisher Syndrome (MFS) is a rare neurological disorder that is considered a variant of Guillain-Barré syndrome. It is characterized by the triad of symptoms including ophthalmoplegia (paralysis of the eye muscles), ataxia (loss of coordination and balance), and areflexia (absence of reflexes). Some patients may also experience weakness or paralysis in the limbs, and some cases may involve bulbar symptoms such as dysphagia (difficulty swallowing) and dysarthria (slurred speech). The syndrome is caused by an immune response that damages the nerves, and it often follows a viral infection. Treatment typically includes supportive care, plasma exchange, or intravenous immunoglobulin therapy to help reduce the severity of the symptoms.

Blepharoptosis is a medical term that refers to the drooping or falling of the upper eyelid. It is usually caused by weakness or paralysis of the muscle that raises the eyelid, known as the levator palpebrae superioris. This condition can be present at birth or acquired later in life due to various factors such as aging, nerve damage, eye surgery complications, or certain medical conditions like myasthenia gravis or brain tumors. Blepharoptosis may obstruct vision and cause difficulty with daily activities, and treatment options include eyedrops, eye patches, or surgical correction.

Ocular motility disorders refer to a group of conditions that affect the movement of the eyes. These disorders can result from nerve damage, muscle dysfunction, or brain injuries. They can cause abnormal eye alignment, limited range of motion, and difficulty coordinating eye movements. Common symptoms include double vision, blurry vision, strabismus (crossed eyes), nystagmus (involuntary eye movement), and difficulty tracking moving objects. Ocular motility disorders can be congenital or acquired and may require medical intervention to correct or manage the condition.

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.

Mitochondrial DNA (mtDNA) is the genetic material present in the mitochondria, which are specialized structures within cells that generate energy. Unlike nuclear DNA, which is present in the cell nucleus and inherited from both parents, mtDNA is inherited solely from the mother.

MtDNA is a circular molecule that contains 37 genes, including 13 genes that encode for proteins involved in oxidative phosphorylation, a process that generates energy in the form of ATP. The remaining genes encode for rRNAs and tRNAs, which are necessary for protein synthesis within the mitochondria.

Mutations in mtDNA can lead to a variety of genetic disorders, including mitochondrial diseases, which can affect any organ system in the body. These mutations can also be used in forensic science to identify individuals and establish biological relationships.

The cavernous sinus is a venous structure located in the middle cranial fossa, which is a depression in the skull that houses several important nerves and blood vessels. The cavernous sinus is situated on either side of the sphenoid bone, near the base of the skull, and it contains several important structures:

* The internal carotid artery, which supplies oxygenated blood to the brain
* The abducens nerve (cranial nerve VI), which controls lateral movement of the eye
* The oculomotor nerve (cranial nerve III), which controls most of the muscles that move the eye
* The trochlear nerve (cranial nerve IV), which controls one of the muscles that moves the eye
* The ophthalmic and maxillary divisions of the trigeminal nerve (cranial nerve V), which transmit sensory information from the face and head

The cavernous sinus is an important structure because it serves as a conduit for several critical nerves and blood vessels. However, it is also vulnerable to various pathological conditions such as thrombosis (blood clots), infection, tumors, or aneurysms, which can lead to serious neurological deficits or even death.

Herpes Zoster Ophthalmicus (HZO) is a type of herpes zoster (shingles) infection that affects the ophthalmic division (V1) of the trigeminal nerve. It is caused by the varicella-zoster virus, which also causes chickenpox. After a person recovers from chickenpox, the virus remains inactive in the body and can reactivate later as shingles, often many years after the initial infection.

When the virus reactivates and affects the ophthalmic division of the trigeminal nerve, it can cause a painful rash on the forehead, nose, and around one eye. The rash may be accompanied by other symptoms such as headache, fever, and fatigue. In some cases, HZO can also affect the eye itself, causing inflammation, corneal ulcers, and vision loss if left untreated.

It is important to seek medical attention promptly if you suspect you have HZO, as early treatment with antiviral medications can help reduce the severity of symptoms and prevent complications.

Exophthalmos is a medical condition that refers to the abnormal protrusion or bulging of one or both eyes beyond the normal orbit (eye socket). This condition is also known as proptosis. Exophthalmos can be caused by various factors, including thyroid eye disease (Graves' ophthalmopathy), tumors, inflammation, trauma, or congenital abnormalities. It can lead to various symptoms such as double vision, eye discomfort, redness, and difficulty closing the eyes. Treatment of exophthalmos depends on the underlying cause and may include medications, surgery, or radiation therapy.

The oculomotor muscles are a group of extraocular muscles that control the movements of the eye. They include:

1. Superior rectus: This muscle is responsible for elevating the eye and helping with inward rotation (intorsion) when looking downwards.
2. Inferior rectus: It depresses the eye and helps with outward rotation (extorsion) when looking upwards.
3. Medial rectus: This muscle adducts, or moves, the eye towards the midline of the face.
4. Inferior oblique: The inferior oblique muscle intorts and elevates the eye.
5. Superior oblique: It extorts and depresses the eye.

These muscles work together to allow for smooth and precise movements of the eyes, enabling tasks such as tracking moving objects, reading, and maintaining visual fixation on a single point in space.

Tolosa-Hunt syndrome is a rare disorder characterized by the inflammation of the nerve structures (including the fifth and sixth cranial nerves) within the cavernous sinus, a venous space near the base of the skull. This inflammation can lead to various symptoms such as:

1. Unilateral or bilateral orbital pain, which may be severe and deep, often radiating around the eye and temple.
2. Ophthalmoplegia (paralysis of the eye muscles), causing double vision (diplopia) and limited eye movement in specific directions.
3. Ptosis (drooping of the eyelid).
4. Other possible symptoms include decreased sensation around the forehead, cheek, or upper jaw, and loss of taste on the anterior part of the tongue.

The exact cause of Tolosa-Hunt syndrome is unknown, but it's believed to be related to an autoimmune response or a non-specific inflammatory process. It can also occur in conjunction with other medical conditions like neoplasms (tumors) or infections. The diagnosis typically involves imaging studies such as MRI and CT scans, along with blood tests and a thorough neurological examination.

Treatment usually includes corticosteroids to reduce inflammation and alleviate symptoms. In some cases, immunosuppressive medications or radiation therapy may be necessary. If left untreated, Tolosa-Hunt syndrome can lead to permanent visual impairment or other neurological deficits.

Diplopia is a medical term that refers to the condition where a person sees two images of a single object. It is commonly known as double vision. This can occur due to various reasons, such as nerve damage or misalignment of the eyes. Diplopia can be temporary or chronic and can affect one or both eyes. If you're experiencing diplopia, it's essential to consult an eye care professional for proper evaluation and treatment.

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.

Mitochondrial myopathies are a group of genetic disorders caused by mutations in the mitochondrial DNA or nuclear DNA that affect the function of the mitochondria, which are the energy-producing structures in cells. These mutations can result in impaired muscle function and other symptoms, depending on the specific type and severity of the disorder.

Mitochondrial myopathies can present at any age and can cause a range of symptoms, including muscle weakness, exercise intolerance, fatigue, muscle pain, and difficulty with coordination and balance. Some people with mitochondrial myopathies may also experience neurological symptoms such as seizures, developmental delays, and hearing or vision loss.

The diagnosis of mitochondrial myopathies typically involves a combination of clinical evaluation, muscle biopsy, genetic testing, and other diagnostic tests to assess mitochondrial function. Treatment is generally supportive and may include physical therapy, medications to manage symptoms, and nutritional support. In some cases, specific therapies such as vitamin or coenzyme Q10 supplementation may be recommended based on the underlying genetic defect.

Mitochondrial diseases are a group of disorders caused by dysfunctions in the mitochondria, which are the energy-producing structures in cells. These diseases can affect people of any age and can manifest in various ways, depending on which organs or systems are affected. Common symptoms include muscle weakness, neurological problems, cardiac disease, diabetes, and vision/hearing loss. Mitochondrial diseases can be inherited from either the mother's or father's side, or they can occur spontaneously due to genetic mutations. They can range from mild to severe and can even be life-threatening in some cases.

Wernicke Encephalopathy is a neuropsychiatric disorder that is caused by a deficiency of thiamine (vitamin B1). It is characterized by a classic triad of symptoms: confusion, oculomotor dysfunction (such as nystagmus and ophthalmoplegia), and gait ataxia. Other symptoms can include memory loss, apathy, and hypothermia.

Wernicke Encephalopathy is most commonly seen in alcoholics due to poor nutrition, but it can also occur in people with conditions that cause malabsorption or increased thiamine requirements, such as AIDS, cancer, and chronic diarrhea. Immediate treatment with thiamine replacement therapy is necessary to prevent progression of the disease and potential permanent neurological damage. If left untreated, Wernicke Encephalopathy can lead to Korsakoff's syndrome, a chronic memory disorder.

Mitochondrial Encephalomyopathies are a group of genetic disorders that primarily affect the mitochondria, which are the energy-producing structures in cells. "Encephalo" refers to the brain, while "myopathy" refers to muscle disease. Therefore, Mitochondrial Encephalomyopathies are conditions that cause both neurological and muscular symptoms due to impaired mitochondrial function.

These disorders can affect any organ in the body, but they primarily impact the brain, nerves, and muscles. Symptoms may include muscle weakness, seizures, developmental delays, hearing loss, vision loss, heart problems, and lactic acidosis (a buildup of lactic acid in the blood).

Mitochondrial Encephalomyopathies can be caused by mutations in either the mitochondrial DNA or nuclear DNA. They are often inherited from the mother, as mitochondria are passed down through the maternal line. However, some cases can also result from new mutations that occur spontaneously.

Due to the complex nature of these disorders and their varying symptoms, diagnosis and treatment can be challenging. Treatment typically focuses on managing specific symptoms and may include medications, dietary changes, and physical therapy.

The abducens nerve, also known as the sixth cranial nerve (CN VI), is a motor nerve that controls the lateral rectus muscle of the eye. This muscle is responsible for moving the eye away from the midline (towards the temple) and enables the eyes to look towards the side while keeping them aligned. Any damage or dysfunction of the abducens nerve can result in strabismus, where the eyes are misaligned and point in different directions, specifically an adduction deficit, also known as abducens palsy or sixth nerve palsy.

The abducens nerve, also known as the sixth cranial nerve, is responsible for controlling the lateral rectus muscle of the eye, which enables the eye to move outward. Abducens nerve diseases refer to conditions that affect this nerve and can result in various symptoms, primarily affecting eye movement.

Here are some medical definitions related to abducens nerve diseases:

1. Abducens Nerve Palsy: A condition characterized by weakness or paralysis of the abducens nerve, causing difficulty in moving the affected eye outward. This results in double vision (diplopia), especially when gazing towards the side of the weakened nerve. Abducens nerve palsy can be congenital, acquired, or caused by various factors such as trauma, tumors, aneurysms, infections, or diseases like diabetes and multiple sclerosis.
2. Sixth Nerve Palsy: Another term for abducens nerve palsy, referring to the weakness or paralysis of the sixth cranial nerve.
3. Internuclear Ophthalmoplegia (INO): A neurological condition affecting eye movement, often caused by a lesion in the medial longitudinal fasciculus (MLF), a bundle of nerve fibers that connects the abducens nucleus with the oculomotor nucleus. INO results in impaired adduction (inward movement) of the eye on the side of the lesion and nystagmus (involuntary eye movements) of the abducting eye on the opposite side when attempting to look towards the side of the lesion.
4. One-and-a-Half Syndrome: A rare neurological condition characterized by a combination of INO and internuclear ophthalmoplegia with horizontal gaze palsy on the same side, caused by damage to both the abducens nerve and the paramedian pontine reticular formation (PPRF). This results in limited or no ability to move the eyes towards the side of the lesion and impaired adduction of the eye on the opposite side.
5. Brainstem Encephalitis: Inflammation of the brainstem, which can affect the abducens nerve and other cranial nerves, leading to various neurological symptoms such as diplopia (double vision), ataxia (loss of balance and coordination), and facial weakness. Brainstem encephalitis can be caused by infectious agents, autoimmune disorders, or paraneoplastic syndromes.
6. Multiple Sclerosis (MS): An autoimmune disorder characterized by inflammation and demyelination of the central nervous system, including the brainstem and optic nerves. MS can cause various neurological symptoms, such as diplopia, nystagmus, and INO, due to damage to the abducens nerve and other cranial nerves.
7. Wernicke's Encephalopathy: A neurological disorder caused by thiamine (vitamin B1) deficiency, often seen in alcoholics or individuals with malnutrition. Wernicke's encephalopathy can affect the brainstem and cause various symptoms such as diplopia, ataxia, confusion, and oculomotor abnormalities.
8. Pontine Glioma: A rare type of brain tumor that arises from the glial cells in the pons (a part of the brainstem). Pontine gliomas can cause various neurological symptoms such as diplopia, facial weakness, and difficulty swallowing due to their location in the brainstem.
9. Brainstem Cavernous Malformation: A benign vascular lesion that arises from the small blood vessels in the brainstem. Brainstem cavernous malformations can cause various neurological symptoms such as diplopia, ataxia, and facial weakness due to their location in the brainstem.
10. Pituitary Adenoma: A benign tumor that arises from the pituitary gland, located at the base of the brain. Large pituitary adenomas can compress the optic nerves and cause various visual symptoms such as diplopia, visual field defects, and decreased vision.
11. Craniopharyngioma: A benign tumor that arises from the remnants of the Rathke's pouch, a structure that gives rise to the anterior pituitary gland. Craniopharyngiomas can cause various neurological and endocrine symptoms such as diplopia, visual field defects, headaches, and hormonal imbalances due to their location near the optic nerves and pituitary gland.
12. Meningioma: A benign tumor that arises from the meninges, the protective covering of the brain and spinal cord. Meningiomas can cause various neurological symptoms such as diplopia, headaches, and seizures depending on their location in the brain or spinal cord.
13. Chordoma: A rare type of malignant tumor that arises from the remnants of the notochord, a structure that gives rise to the spine during embryonic development. Chordomas can cause various neurological and endocrine symptoms such as diplopia, visual field defects, headaches, and hormonal imbalances due to their location near the brainstem and spinal cord.
14. Metastatic Brain Tumors: Malignant tumors that spread from other parts of the body to the brain. Metastatic brain tumors can cause various neurological symptoms such as diplopia, headaches, seizures, and cognitive impairment depending on their location in the brain.
15. Other Rare Brain Tumors: There are many other rare types of brain tumors that can cause diplopia or other neurological symptoms, including gliomas, ependymomas, pineal region tumors, and others. These tumors require specialized diagnosis and treatment by neuro-oncologists and neurosurgeons with expertise in these rare conditions.

In summary, diplopia can be caused by various brain tumors, including pituitary adenomas, meningiomas, chordomas, metastatic brain tumors, and other rare types of tumors. It is important to seek medical attention promptly if you experience diplopia or other neurological symptoms, as early diagnosis and treatment can improve outcomes and quality of life.

Adenine Nucleotide Translocator 1 (ANT1) is a protein found in the inner mitochondrial membrane of cells. It plays a crucial role in cellular energy metabolism by facilitating the exchange of adenosine diphosphate (ADP) and adenosine triphosphate (ATP) across the mitochondrial membrane.

In simpler terms, ANT1 helps to transport ATP, which is a major source of energy for cells, out of the mitochondria and exchange it for ADP, which can be converted back into ATP through cellular respiration. This process is essential for maintaining the energy balance within the cell and supporting various physiological functions.

Mutations in the gene that encodes ANT1 have been associated with certain mitochondrial disorders, such as autosomal recessive progressive external ophthalmoplegia (arPEO) and maternally inherited diabetes and deafness (MIDD). These genetic conditions can result in a range of symptoms, including muscle weakness, exercise intolerance, and neurological problems.

Cranial nerve diseases refer to conditions that affect the cranial nerves, which are a set of 12 pairs of nerves that originate from the brainstem and control various functions in the head and neck. These functions include vision, hearing, taste, smell, movement of the eyes and face, and sensation in the face.

Diseases of the cranial nerves can result from a variety of causes, including injury, infection, inflammation, tumors, or degenerative conditions. The specific symptoms that a person experiences will depend on which cranial nerve is affected and how severely it is damaged.

For example, damage to the optic nerve (cranial nerve II) can cause vision loss or visual disturbances, while damage to the facial nerve (cranial nerve VII) can result in weakness or paralysis of the face. Other common symptoms of cranial nerve diseases include pain, numbness, tingling, and hearing loss.

Treatment for cranial nerve diseases varies depending on the underlying cause and severity of the condition. In some cases, medication or surgery may be necessary to treat the underlying cause and relieve symptoms. Physical therapy or rehabilitation may also be recommended to help individuals regain function and improve their quality of life.

Ataxia is a medical term that refers to a group of disorders affecting coordination, balance, and speech. It is characterized by a lack of muscle control during voluntary movements, causing unsteady or awkward movements, and often accompanied by tremors. Ataxia can affect various parts of the body, such as the limbs, trunk, eyes, and speech muscles. The condition can be congenital or acquired, and it can result from damage to the cerebellum, spinal cord, or sensory nerves. There are several types of ataxia, including hereditary ataxias, degenerative ataxias, cerebellar ataxias, and acquired ataxias, each with its own specific causes, symptoms, and prognosis. Treatment for ataxia typically focuses on managing symptoms and improving quality of life, as there is no cure for most forms of the disorder.

The oculomotor nerve, also known as the third cranial nerve (CN III), is a motor nerve that originates from the midbrain. It controls the majority of the eye muscles, including the levator palpebrae superioris muscle that raises the upper eyelid, and the extraocular muscles that enable various movements of the eye such as looking upward, downward, inward, and outward. Additionally, it carries parasympathetic fibers responsible for pupillary constriction and accommodation (focusing on near objects). Damage to this nerve can result in various ocular motor disorders, including strabismus, ptosis, and pupillary abnormalities.

Pathological nystagmus is an abnormal, involuntary movement of the eyes that can occur in various directions (horizontal, vertical, or rotatory) and can be rhythmical or arrhythmic. It is typically a result of a disturbance in the vestibular system, central nervous system, or ocular motor pathways. Pathological nystagmus can cause visual symptoms such as blurred vision, difficulty with fixation, and oscillopsia (the sensation that one's surroundings are moving). The type, direction, and intensity of the nystagmus may vary depending on the underlying cause, which can include conditions such as brainstem or cerebellar lesions, multiple sclerosis, drug toxicity, inner ear disorders, and congenital abnormalities.

Muscular diseases, also known as myopathies, refer to a group of conditions that affect the functionality and health of muscle tissue. These diseases can be inherited or acquired and may result from inflammation, infection, injury, or degenerative processes. They can cause symptoms such as weakness, stiffness, cramping, spasms, wasting, and loss of muscle function.

Examples of muscular diseases include:

1. Duchenne Muscular Dystrophy (DMD): A genetic disorder that results in progressive muscle weakness and degeneration due to a lack of dystrophin protein.
2. Myasthenia Gravis: An autoimmune disease that causes muscle weakness and fatigue, typically affecting the eyes and face, throat, and limbs.
3. Inclusion Body Myositis (IBM): A progressive muscle disorder characterized by muscle inflammation and wasting, typically affecting older adults.
4. Polymyositis: An inflammatory myopathy that causes muscle weakness and inflammation throughout the body.
5. Metabolic Myopathies: A group of inherited disorders that affect muscle metabolism, leading to exercise intolerance, muscle weakness, and other symptoms.
6. Muscular Dystonias: Involuntary muscle contractions and spasms that can cause abnormal postures or movements.

It is important to note that muscular diseases can have a significant impact on an individual's quality of life, mobility, and overall health. Proper diagnosis and treatment are crucial for managing symptoms and improving outcomes.

Orbital neoplasms refer to abnormal growths or tumors that develop in the orbit, which is the bony cavity that contains the eyeball, muscles, nerves, fat, and blood vessels. These neoplasms can be benign (non-cancerous) or malignant (cancerous), and they can arise from various types of cells within the orbit.

Orbital neoplasms can cause a variety of symptoms depending on their size, location, and rate of growth. Common symptoms include protrusion or displacement of the eyeball, double vision, limited eye movement, pain, swelling, and numbness in the face. In some cases, orbital neoplasms may not cause any noticeable symptoms, especially if they are small and slow-growing.

There are many different types of orbital neoplasms, including:

1. Optic nerve glioma: a rare tumor that arises from the optic nerve's supportive tissue.
2. Orbital meningioma: a tumor that originates from the membranes covering the brain and extends into the orbit.
3. Lacrimal gland tumors: benign or malignant growths that develop in the lacrimal gland, which produces tears.
4. Orbital lymphangioma: a non-cancerous tumor that arises from the lymphatic vessels in the orbit.
5. Rhabdomyosarcoma: a malignant tumor that develops from the skeletal muscle cells in the orbit.
6. Metastatic tumors: cancerous growths that spread to the orbit from other parts of the body, such as the breast, lung, or prostate.

The diagnosis and treatment of orbital neoplasms depend on several factors, including the type, size, location, and extent of the tumor. Imaging tests, such as CT scans and MRI, are often used to visualize the tumor and determine its extent. A biopsy may also be performed to confirm the diagnosis and determine the tumor's type and grade. Treatment options include surgery, radiation therapy, chemotherapy, or a combination of these approaches.

Diffuse cerebral sclerosis of Schilder, also known as Schilder's disease, is a rare inflammatory demyelinating disorder of the central nervous system. It primarily affects children and young adults, but can occur at any age. The condition is characterized by widespread destruction of the myelin sheath, which surrounds and protects nerve fibers in the brain.

The hallmark feature of Schilder's disease is the presence of multiple, large, symmetrical lesions in the white matter of both cerebral hemispheres. These lesions are typically located in the parieto-occipital regions of the brain and can extend to involve other areas as well.

The symptoms of Schilder's disease vary depending on the location and extent of the lesions, but may include:

* Progressive intellectual decline
* Seizures
* Visual disturbances
* Weakness or paralysis on one side of the body (hemiparesis)
* Loss of sensation in various parts of the body
* Speech difficulties
* Behavioral changes, such as irritability, mood swings, and depression

The exact cause of Schilder's disease is not known, but it is believed to be an autoimmune disorder, in which the body's own immune system mistakenly attacks the myelin sheath. There is no cure for Schilder's disease, and treatment typically involves corticosteroids or other immunosuppressive therapies to reduce inflammation and slow the progression of the disease. Despite treatment, many patients with Schilder's disease experience significant disability and may require long-term care.

Orbital pseudotumor, also known as orbital inflammatory syndrome or idiopathic orbital inflammation, is a non-specific term used to describe a group of conditions characterized by inflammation in the orbit (the bony cavity surrounding the eye) without any identifiable cause. It is not a true tumor, but rather an inflammatory reaction that can mimic the symptoms and signs of a tumor.

The condition can affect people of any age, although it is more common in middle-aged adults. The exact cause of orbital pseudotumor is unknown, but it is believed to be related to an abnormal immune response or inflammation triggered by various factors such as infections, trauma, or autoimmune disorders.

Symptoms of orbital pseudotumor may include eye pain, redness, swelling, protrusion of the eyeball (proptosis), double vision, and decreased vision. Diagnostic tests such as imaging studies (CT or MRI scans) and biopsy may be used to rule out other causes of orbital inflammation. Treatment typically involves corticosteroids to reduce inflammation, although other immunosuppressive medications may be necessary in severe cases. In some cases, the condition may resolve on its own without treatment.

Mitochondria in muscle, also known as the "powerhouses" of the cell, are organelles that play a crucial role in generating energy for muscle cells through a process called cellular respiration. They convert the chemical energy found in glucose and oxygen into ATP (adenosine triphosphate), which is the main source of energy used by cells.

Muscle cells contain a high number of mitochondria due to their high energy demands for muscle contraction and relaxation. The number and size of mitochondria in muscle fibers can vary depending on the type of muscle fiber, with slow-twitch, aerobic fibers having more numerous and larger mitochondria than fast-twitch, anaerobic fibers.

Mitochondrial dysfunction has been linked to various muscle disorders, including mitochondrial myopathies, which are characterized by muscle weakness, exercise intolerance, and other symptoms related to impaired energy production in the muscle cells.

Intestinal pseudo-obstruction, also known as paralytic ileus or functional obstruction, is a gastrointestinal motility disorder characterized by the absence of mechanical obstruction in the intestines, but with symptoms mimicking a mechanical small bowel obstruction. These symptoms may include abdominal distention, cramping, nausea, vomiting, and constipation or difficulty passing stools.

The condition is caused by impaired intestinal motility due to dysfunction of the nerves or muscles that control the movement of food and waste through the digestive system. It can be a chronic or acute condition and may occur as a primary disorder or secondary to other medical conditions, such as surgery, trauma, infections, metabolic disorders, neurological diseases, or certain medications.

Diagnosis of intestinal pseudo-obstruction typically involves imaging studies, such as X-rays or CT scans, to rule out mechanical obstruction and confirm the presence of dilated bowel loops. Manometry and other specialized tests may also be used to assess intestinal motility. Treatment options include medications to stimulate intestinal motility, dietary modifications, and in severe cases, surgery or intravenous nutrition.

Electrooculography (EOG) is a technique for measuring the resting potential of the eye and the changes in this potential that occur with eye movements. It involves placing electrodes near the eyes to detect the small electric fields generated by the movement of the eyeball within the surrounding socket. This technique is used in research and clinical settings to study eye movements and their control, as well as in certain diagnostic applications such as assessing the function of the oculomotor system in patients with neurological disorders.

Neuromuscular diseases are a group of disorders that involve the peripheral nervous system, which includes the nerves and muscles outside of the brain and spinal cord. These conditions can affect both children and adults, and they can be inherited or acquired. Neuromuscular diseases can cause a wide range of symptoms, including muscle weakness, numbness, tingling, pain, cramping, and twitching. Some common examples of neuromuscular diseases include muscular dystrophy, amyotrophic lateral sclerosis (ALS), peripheral neuropathy, and myasthenia gravis. The specific symptoms and severity of these conditions can vary widely depending on the underlying cause and the specific muscles and nerves that are affected. Treatment for neuromuscular diseases may include medications, physical therapy, assistive devices, or surgery, depending on the individual case.

Eye movements, also known as ocular motility, refer to the voluntary or involuntary motion of the eyes that allows for visual exploration of our environment. There are several types of eye movements, including:

1. Saccades: rapid, ballistic movements that quickly shift the gaze from one point to another.
2. Pursuits: smooth, slow movements that allow the eyes to follow a moving object.
3. Vergences: coordinated movements of both eyes in opposite directions, usually in response to a three-dimensional stimulus.
4. Vestibulo-ocular reflex (VOR): automatic eye movements that help stabilize the gaze during head movement.
5. Optokinetic nystagmus (OKN): rhythmic eye movements that occur in response to large moving visual patterns, such as when looking out of a moving vehicle.

Abnormalities in eye movements can indicate neurological or ophthalmological disorders and are often assessed during clinical examinations.

Gangliosides are a type of complex lipid molecule known as sialic acid-containing glycosphingolipids. They are predominantly found in the outer leaflet of the cell membrane, particularly in the nervous system. Gangliosides play crucial roles in various biological processes, including cell recognition, signal transduction, and cell adhesion. They are especially abundant in the ganglia (nerve cell clusters) of the peripheral and central nervous systems, hence their name.

Gangliosides consist of a hydrophobic ceramide portion and a hydrophilic oligosaccharide chain that contains one or more sialic acid residues. The composition and structure of these oligosaccharide chains can vary significantly among different gangliosides, leading to the classification of various subtypes, such as GM1, GD1a, GD1b, GT1b, and GQ1b.

Abnormalities in ganglioside metabolism or expression have been implicated in several neurological disorders, including Parkinson's disease, Alzheimer's disease, and various lysosomal storage diseases like Tay-Sachs and Gaucher's diseases. Additionally, certain bacterial toxins, such as botulinum neurotoxin and tetanus toxin, target gangliosides to gain entry into neuronal cells, causing their toxic effects.

In medical terms, the orbit refers to the bony cavity or socket in the skull that contains and protects the eye (eyeball) and its associated structures, including muscles, nerves, blood vessels, fat, and the lacrimal gland. The orbit is made up of several bones: the frontal bone, sphenoid bone, zygomatic bone, maxilla bone, and palatine bone. These bones form a pyramid-like shape that provides protection for the eye while also allowing for a range of movements.

A syndrome, in medical terms, is a set of symptoms that collectively indicate or characterize a disease, disorder, or underlying pathological process. It's essentially a collection of signs and/or symptoms that frequently occur together and can suggest a particular cause or condition, even though the exact physiological mechanisms might not be fully understood.

For example, Down syndrome is characterized by specific physical features, cognitive delays, and other developmental issues resulting from an extra copy of chromosome 21. Similarly, metabolic syndromes like diabetes mellitus type 2 involve a group of risk factors such as obesity, high blood pressure, high blood sugar, and abnormal cholesterol or triglyceride levels that collectively increase the risk of heart disease, stroke, and diabetes.

It's important to note that a syndrome is not a specific diagnosis; rather, it's a pattern of symptoms that can help guide further diagnostic evaluation and management.

Facial paralysis is a loss of facial movement due to damage or dysfunction of the facial nerve (cranial nerve VII). This nerve controls the muscles involved in facial expressions, such as smiling, frowning, and closing the eyes. Damage to one side of the facial nerve can cause weakness or paralysis on that side of the face.

Facial paralysis can result from various conditions, including:

1. Bell's palsy - an idiopathic (unknown cause) inflammation of the facial nerve
2. Trauma - skull fractures, facial injuries, or surgical trauma to the facial nerve
3. Infections - Lyme disease, herpes zoster (shingles), HIV/AIDS, or bacterial infections like meningitis
4. Tumors - benign or malignant growths that compress or invade the facial nerve
5. Stroke - damage to the brainstem where the facial nerve originates
6. Congenital conditions - some people are born with facial paralysis due to genetic factors or birth trauma

Symptoms of facial paralysis may include:

* Inability to move one or more parts of the face, such as the eyebrows, eyelids, mouth, or cheeks
* Drooping of the affected side of the face
* Difficulty closing the eye on the affected side
* Changes in saliva and tear production
* Altered sense of taste
* Pain around the ear or jaw
* Speech difficulties due to weakened facial muscles

Treatment for facial paralysis depends on the underlying cause. In some cases, such as Bell's palsy, spontaneous recovery may occur within a few weeks to months. However, physical therapy, medications, and surgical interventions might be necessary in other situations to improve function and minimize complications.

The pons is a part of the brainstem that lies between the medulla oblongata and the midbrain. Its name comes from the Latin word "ponte" which means "bridge," as it serves to connect these two regions of the brainstem. The pons contains several important structures, including nerve fibers that carry signals between the cerebellum (the part of the brain responsible for coordinating muscle movements) and the rest of the nervous system. It also contains nuclei (clusters of neurons) that help regulate various functions such as respiration, sleep, and facial movements.

The trochlear nerve, also known as the fourth cranial nerve (CN IV), is responsible for controlling the movement of the eye. It innervates the superior oblique muscle, which helps in depressing and rotating the eye downwards and outwards. Trochlear nerve diseases refer to conditions that affect this nerve and impair its function, leading to symptoms such as double vision (diplopia), vertical misalignment of the eyes, and difficulty with depth perception.

Trochlear nerve diseases can be caused by various factors, including trauma, compression, inflammation, infection, or tumors. Some common conditions that affect the trochlear nerve include:

1. Trochlear nerve palsy: This is a weakness or paralysis of the trochlear nerve, which can cause vertical and torsional diplopia, especially when looking downwards or to the side. It can be congenital or acquired due to trauma, compression, or other causes.
2. Aneurysm: Aneurysms in the vicinity of the trochlear nerve can compress or damage it, leading to palsy and diplopia.
3. Meningitis: Inflammation of the meninges (the membranes surrounding the brain and spinal cord) due to infection or other causes can affect the trochlear nerve and cause palsy.
4. Multiple sclerosis (MS): This is a chronic autoimmune disease that affects the central nervous system, including the cranial nerves. MS can cause demyelination of the trochlear nerve, leading to palsy and diplopia.
5. Diabetes: People with diabetes are at risk of developing diabetic neuropathy, which can affect any peripheral nerve, including the trochlear nerve.
6. Tumors: Space-occupying lesions in the brain or skull base, such as meningiomas, schwannomas, or pituitary adenomas, can compress the trochlear nerve and cause palsy.

The diagnosis of trochlear nerve diseases involves a thorough neurological examination, including assessment of eye movements and alignment. Imaging studies such as MRI or CT scans may be ordered to identify any structural lesions causing compression or damage to the nerve. Treatment depends on the underlying cause and may involve surgical intervention, medication, or observation.

Transverse Myelitis is a neurological disorder that involves inflammation of the spinal cord, leading to damage in both sides of the cord. This results in varying degrees of motor, sensory, and autonomic dysfunction, typically defined by the level of the spine that's affected. Symptoms may include a sudden onset of lower back pain, muscle weakness, paraesthesia or loss of sensation, and bowel/bladder dysfunction. The exact cause is often unknown but can be associated with infections, autoimmune disorders, or other underlying conditions.

Medical Definition:

Magnetic Resonance Imaging (MRI) is a non-invasive diagnostic imaging technique that uses a strong magnetic field and radio waves to create detailed cross-sectional or three-dimensional images of the internal structures of the body. The patient lies within a large, cylindrical magnet, and the scanner detects changes in the direction of the magnetic field caused by protons in the body. These changes are then converted into detailed images that help medical professionals to diagnose and monitor various medical conditions, such as tumors, injuries, or diseases affecting the brain, spinal cord, heart, blood vessels, joints, and other internal organs. MRI does not use radiation like computed tomography (CT) scans.

DNA-directed DNA polymerase is a type of enzyme that synthesizes new strands of DNA by adding nucleotides to an existing DNA template in a 5' to 3' direction. These enzymes are essential for DNA replication, repair, and recombination. They require a single-stranded DNA template, a primer with a free 3' hydroxyl group, and the four deoxyribonucleoside triphosphates (dNTPs) as substrates to carry out the polymerization reaction.

DNA polymerases also have proofreading activity, which allows them to correct errors that occur during DNA replication by removing mismatched nucleotides and replacing them with the correct ones. This helps ensure the fidelity of the genetic information passed from one generation to the next.

There are several different types of DNA polymerases, each with specific functions and characteristics. For example, DNA polymerase I is involved in both DNA replication and repair, while DNA polymerase III is the primary enzyme responsible for DNA replication in bacteria. In eukaryotic cells, DNA polymerase alpha, beta, gamma, delta, and epsilon have distinct roles in DNA replication, repair, and maintenance.

Orbital diseases refer to a group of medical conditions that affect the orbit, which is the bony cavity in the skull that contains the eye, muscles, nerves, fat, and blood vessels. These diseases can cause various symptoms such as eyelid swelling, protrusion or displacement of the eyeball, double vision, pain, and limited extraocular muscle movement.

Orbital diseases can be broadly classified into inflammatory, infectious, neoplastic (benign or malignant), vascular, traumatic, and congenital categories. Some examples of orbital diseases include:

* Orbital cellulitis: a bacterial or fungal infection that causes swelling and inflammation in the orbit
* Graves' disease: an autoimmune disorder that affects the thyroid gland and can cause protrusion of the eyeballs (exophthalmos)
* Orbital tumors: benign or malignant growths that develop in the orbit, such as optic nerve gliomas, lacrimal gland tumors, and lymphomas
* Carotid-cavernous fistulas: abnormal connections between the carotid artery and cavernous sinus, leading to pulsatile proptosis and other symptoms
* Orbital fractures: breaks in the bones surrounding the orbit, often caused by trauma
* Congenital anomalies: structural abnormalities present at birth, such as craniofacial syndromes or dermoid cysts.

Proper diagnosis and management of orbital diseases require a multidisciplinary approach involving ophthalmologists, neurologists, radiologists, and other specialists.

Guillain-Barré syndrome (GBS) is a rare autoimmune disorder in which the body's immune system mistakenly attacks the peripheral nervous system, leading to muscle weakness, tingling sensations, and sometimes paralysis. The peripheral nervous system includes the nerves that control our movements and transmit signals from our skin, muscles, and joints to our brain.

The onset of GBS usually occurs after a viral or bacterial infection, such as respiratory or gastrointestinal infections, or following surgery, vaccinations, or other immune system triggers. The exact cause of the immune response that leads to GBS is not fully understood.

GBS typically progresses rapidly over days or weeks, with symptoms reaching their peak within 2-4 weeks after onset. Most people with GBS experience muscle weakness that starts in the lower limbs and spreads upward to the upper body, arms, and face. In severe cases, the diaphragm and chest muscles may become weakened, leading to difficulty breathing and requiring mechanical ventilation.

The diagnosis of GBS is based on clinical symptoms, nerve conduction studies, and sometimes cerebrospinal fluid analysis. Treatment typically involves supportive care, such as pain management, physical therapy, and respiratory support if necessary. In addition, plasma exchange (plasmapheresis) or intravenous immunoglobulin (IVIG) may be used to reduce the severity of symptoms and speed up recovery.

While most people with GBS recover completely or with minimal residual symptoms, some may experience long-term disability or require ongoing medical care. The prognosis for GBS varies depending on the severity of the illness and the individual's age and overall health.

Paranasal sinus diseases refer to a group of medical conditions that affect the paranasal sinuses, which are air-filled cavities located within the skull near the nasal cavity. These sinuses include the maxillary, frontal, ethmoid, and sphenoid sinuses.

Paranasal sinus diseases can be caused by a variety of factors, including viral, bacterial, or fungal infections, allergies, structural abnormalities, or autoimmune disorders. Some common paranasal sinus diseases include:

1. Sinusitis: Inflammation or infection of the sinuses, which can cause symptoms such as nasal congestion, thick nasal discharge, facial pain or pressure, and reduced sense of smell.
2. Nasal polyps: Soft, benign growths that develop in the lining of the nasal passages or sinuses, which can obstruct airflow and cause difficulty breathing through the nose.
3. Sinonasal tumors: Abnormal growths that can be benign or malignant, which can cause symptoms such as nasal congestion, facial pain, and bleeding from the nose.
4. Sinus cysts: Fluid-filled sacs that form in the sinuses, which can cause symptoms similar to those of sinusitis.
5. Fungal sinusitis: Infection of the sinuses with fungi, which can cause symptoms such as nasal congestion, facial pain, and thick, discolored mucus.

Treatment for paranasal sinus diseases depends on the underlying cause and severity of the condition. Treatment options may include medications, such as antibiotics, antihistamines, or corticosteroids, as well as surgical intervention in more severe cases.

Cerebellar ataxia is a type of ataxia, which refers to a group of disorders that cause difficulties with coordination and movement. Cerebellar ataxia specifically involves the cerebellum, which is the part of the brain responsible for maintaining balance, coordinating muscle movements, and regulating speech and eye movements.

The symptoms of cerebellar ataxia may include:

* Unsteady gait or difficulty walking
* Poor coordination of limb movements
* Tremors or shakiness, especially in the hands
* Slurred or irregular speech
* Abnormal eye movements, such as nystagmus (rapid, involuntary movement of the eyes)
* Difficulty with fine motor tasks, such as writing or buttoning a shirt

Cerebellar ataxia can be caused by a variety of underlying conditions, including:

* Genetic disorders, such as spinocerebellar ataxia or Friedreich's ataxia
* Brain injury or trauma
* Stroke or brain hemorrhage
* Infections, such as meningitis or encephalitis
* Exposure to toxins, such as alcohol or certain medications
* Tumors or other growths in the brain

Treatment for cerebellar ataxia depends on the underlying cause. In some cases, there may be no cure, and treatment is focused on managing symptoms and improving quality of life. Physical therapy, occupational therapy, and speech therapy can help improve coordination, balance, and communication skills. Medications may also be used to treat specific symptoms, such as tremors or muscle spasticity. In some cases, surgery may be recommended to remove tumors or repair damage to the brain.

Prednisolone is a synthetic glucocorticoid drug, which is a class of steroid hormones. It is commonly used in the treatment of various inflammatory and autoimmune conditions due to its potent anti-inflammatory and immunosuppressive effects. Prednisolone works by binding to specific receptors in cells, leading to changes in gene expression that reduce the production of substances involved in inflammation, such as cytokines and prostaglandins.

Prednisolone is available in various forms, including tablets, syrups, and injectable solutions. It can be used to treat a wide range of medical conditions, including asthma, rheumatoid arthritis, inflammatory bowel disease, allergies, skin conditions, and certain types of cancer.

Like other steroid medications, prednisolone can have significant side effects if used in high doses or for long periods of time. These may include weight gain, mood changes, increased risk of infections, osteoporosis, diabetes, and adrenal suppression. As a result, the use of prednisolone should be closely monitored by a healthcare professional to ensure that its benefits outweigh its risks.

A fatal outcome is a term used in medical context to describe a situation where a disease, injury, or illness results in the death of an individual. It is the most severe and unfortunate possible outcome of any medical condition, and is often used as a measure of the severity and prognosis of various diseases and injuries. In clinical trials and research, fatal outcome may be used as an endpoint to evaluate the effectiveness and safety of different treatments or interventions.

Myasthenia Gravis is a long-term autoimmune neuromuscular disorder that leads to muscle weakness. It occurs when communication between nerves and muscles is disrupted at the nerve endings, resulting in fewer impulses being transmitted to activate the muscles. This results in muscle weakness and rapid fatigue. The condition can affect any voluntary muscle, but it most commonly affects muscles of the eyes, face, throat, and limbs. Symptoms may include drooping eyelids (ptosis), double vision (diplopia), difficulty swallowing, slurred speech, and weakness in the arms and legs. The severity of symptoms can vary greatly from person to person, ranging from mild to life-threatening.

The disorder is caused by an abnormal immune system response that produces antibodies against the acetylcholine receptors in the postsynaptic membrane of the neuromuscular junction. These antibodies block or destroy the receptors, which leads to a decrease in the number of available receptors for nerve impulses to activate the muscle fibers.

Myasthenia Gravis can be treated with medications that improve communication between nerves and muscles, such as cholinesterase inhibitors, immunosuppressants, and plasmapheresis or intravenous immunoglobulin (IVIG) to remove the harmful antibodies from the blood. With proper treatment, many people with Myasthenia Gravis can lead normal or nearly normal lives.

Internuclear ophthalmoplegia (INO) is a disorder of conjugate lateral gaze in which the affected eye shows impairment of ... "Internuclear Ophthalmoplegia". The Lecturio Medical Concept Library. Retrieved 7 July 2021. (Articles with short description, ... Lana MA, Moreira PR, Neves LB (December 1990). "Wall-eyed bilateral internuclear ophthalmoplegia (Webino syndrome) and ... Multiple sclerosis One and a half syndrome "Internuclear Ophtalmoplegia". Keane JR (May 2005). "Internuclear ophthalmoplegia: ...
Supranuclear ophthalmoplegia is a condition that affects the movement of the eyes. ... Supranuclear ophthalmoplegia is a condition that affects the movement of the eyes. ... supranuclear ophthalmoplegia; Whipple disease - supranuclear ophthalmoplegia; Dementia - supranuclear ophthalmoplegia ... Progressive supranuclear palsy - supranuclear ophthalmoplegia; Encephalitis - supranuclear ophthalmoplegia; ...
Chronic progressive external ophthalmoplegia (CPEO) is a disorder characterized by slowly progressive paralysis of the ... Chronic progressive external ophthalmoplegia (CPEO), also known as progressive external ophthalmoplegia (PEO), is a disorder ... encoded search term (Chronic Progressive External Ophthalmoplegia (CPEO)) and Chronic Progressive External Ophthalmoplegia ( ... Chronic Progressive External Ophthalmoplegia (CPEO). Updated: Mar 06, 2023 * Author: Michael Mercandetti, MD, MBA, FACS; Chief ...
Diseases associated with ophthalmoplegia are ocular myopathy, which affects muscles, and internuclear ophthalmoplegia, a ... Extractions: 1. Introduction ~ g R h A ] Ø Ç Ì ª Þ @ « i s « O á Ø á (chronic progressive external ophthalmoplegia) Kearns- ... Extractions: Definition Ophthalmoplegia is a paralysis or weakness of one or more of the muscles that control eye movement. The ... Ophthalmoplegia As with most chronic neurologic diseases, mortality increases with disability. Progressiveexternal ...
In progressive external ophthalmoplegia with autosomal dominant inheritance, multiple mitochondrial DNA deletions have been ... Sporadic progressive external ophthalmoplegia and Kearns-Sayre syndrome are usually associated with single large-scale ... Sporadic progressive external ophthalmoplegia and Kearns-Sayre syndrome are usually associated with single large-scale ... In progressive external ophthalmoplegia with autosomal dominant inheritance, multiple mitochondrial DNA deletions have been ...
Ophthalmoplegia. Paralysis or weakness of the eye muscles. It is often caued by neurological disorders. It causes limitation of ...
Early-onset ophthalmoplegia, cervical dyskinesia, and lower extremity weakness due to partial deletion of chromosome 16: A case ... Early-onset ophthalmoplegia, cervical dyskinesia, and lower extremity weakness due to partial deletion of chromosome 16: A case ... Citation: Xu M, Jiang J, He Y, Gu WY, Jin B. Early-onset ophthalmoplegia, cervical dyskinesia, and lower extremity weakness due ... Xu M, Jiang J, He Y, Gu WY, Jin B. Early-onset ophthalmoplegia, cervical dyskinesia, and lower extremity weakness due to ...
Frontalis sling operation using silicone rod for the correction of ptosis in chronic progressive external ophthalmoplegia ... Frontalis sling operation using silicone rod for the correction of ptosis in chronic progressive external ophthalmoplegia ...
Internuclear Ophthalmoplegia - Learn about the causes, symptoms, diagnosis & treatment from the MSD Manuals - Medical Consumer ... People with internuclear ophthalmoplegia may have double vision when they look to the side but may not have double vision when ... In internuclear ophthalmoplegia and one-and-a-half syndrome, the eyes can turn inward when the person looks inward (as when ... People with internuclear ophthalmoplegia or one-and-a-half syndrome may have double vision when they look in certain directions ...
He by no means developed ophthalmoplegia or ataxia. Magnetic resonance imaging of the brain showed contrast enhancement in the ... It is seen as a ophthalmoplegia, areflexia, and ataxia [2]. Our individual under no circumstances developed either ataxia or ... However, isolated bilateral ptosis without ophthalmoplegia is usually a rare manifestation, and isolated unilateral ptosis ... However, isolated bilateral ptosis without ophthalmoplegia is usually a rare manifestation, and isolated unilateral ptosis ...
Diplopia or ophthalmoplegia answers are found in the Diagnosaurus powered by Unbound Medicine. Available for iPhone, iPad, ... Diplopia or Ophthalmoplegia [Internet]. In: Diagnosaurus. McGraw-Hill Education; 2014. [cited 2023 December 08]. Available from ... Zeiger, Roni F.. "Diplopia or Ophthalmoplegia." Diagnosaurus, 4th ed., McGraw-Hill Education, 2014. Medicine Central, im. ... unboundmedicine.com/medicine/view/Diagnosaurus/114386/all/Diplopia_or_ophthalmoplegia. Zeiger RFR. Diplopia or ophthalmoplegia ...
Information on Chronic progressive external ophthalmoplegia, which may include symptoms, causes, inheritance, treatments, ... Is chronic progressive external ophthalmoplegia found in any other conditions? Chronic progressive external ophthalmoplegia ( ... Is chronic progressive external ophthalmoplegia inherited? Chronic progressive external ophthalmoplegia (CPEO) can be inherited ... Chronic progressive external ophthalmoplegia (CPEO) can be an isolated condition, or it can occur as part of other underlying ...
... describes how to differentiate internuclear ophthalmoplegia from third nerve palsy. ... Andrew Lee, MD, describes how to differentiate internuclear ophthalmoplegia from third nerve palsy. ...
Chronic progressive external ophthalmoplegia (CPEO) is a disorder characterized by slowly progressive paralysis of the ... encoded search term (Chronic Progressive External Ophthalmoplegia) and Chronic Progressive External Ophthalmoplegia What to ... Chronic Progressive External Ophthalmoplegia. Updated: Jun 20, 2016 * Author: Michael Mercandetti, MD, MBA, FACS; Chief Editor ... Chronic progressive external ophthalmoplegia with inflammatory myopathy. Int J Clin Exp Pathol. 2014. 7 (12):8887-92. [QxMD ...
Congenital multicore myopathy with external ophthalmoplegia. Get in touch with RARE Concierge.. Contact RARE Concierge ... Congenital multicore myopathy with external ophthalmoplegia. Related Disorders. Multiminicore myopathy. Disorder Group. ... Congenital multicore myopathy with external ophthalmoplegia?. Our RARE Concierge Services Guides are available to assist you by ...
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So, for Ophthalmoplegia [กล้ามเนื้อตาอ่อนแรง], it is mandatory to catch up with the expert cosmetic surgeon and get
Ptosis and progressive external ophthalmoplegia are the outstanding features of this form of external ophthalmoplegia. These ... ANT1, Twinkle, POLG, and TP: new genes open our eyes to ophthalmoplegia. Hirano M, DiMauro S. ANT1, Twinkle, POLG, and TP: new ... External ophthalmoplegia may also result from mutations in POLG (most common), and in C10ORF2. ... Hirano M, DiMauro S. ANT1, Twinkle, POLG, and TP: new genes open our eyes to ophthalmoplegia. Neurology. 2001 Dec 26;57(12): ...
Autosomal recessive progressive external ophthalmoplegia(PEOB1). MedGen UID: 340509. •Concept ID: C1850303. •. Disease or ... Autosomal Recessive Progressive External Ophthalmoplegia (arPEO); PEOB1. SNOMED CT: Autosomal recessive progressive external ... Follow this link to review classifications for Autosomal recessive progressive external ophthalmoplegia in Orphanet. ... Identification of two novel RRM2B variants associated with autosomal recessive progressive external ophthalmoplegia in a family ...
Ocular motility findings in chronic progressive external ophthalmoplegia. Lookup NU author(s): Dr Terence Smith, Dr Andrew ... Method: We studied 25 patients with chronic progressive external ophthalmoplegia. In each case muscle biopsies were consistent ... Aims: To characterise the ocular motility features of chronic progressive external ophthalmoplegia by quantitative and ...
Ramsay Hunt syndrome is a rare neurological condition that causes facial paralysis. Find out how it affects the eyes, mouth and ears.
Ophthalmoplegia in treated polymyalgia rheumatica and healed giant cell arteritis. / Brilakis, Harilaos S.; Lee, Andrew G. ... Brilakis, H. S., & Lee, A. G. (1998). Ophthalmoplegia in treated polymyalgia rheumatica and healed giant cell arteritis. ... Brilakis, HS & Lee, AG 1998, Ophthalmoplegia in treated polymyalgia rheumatica and healed giant cell arteritis, Strabismus, ... Brilakis, Harilaos S. ; Lee, Andrew G. / Ophthalmoplegia in treated polymyalgia rheumatica and healed giant cell arteritis. In ...
PROGRESSIVE EXTERNAL OPHTHALMOPLEGIA WITH MITOCHONDRIAL DNA DELETIONS, AUTOSOMAL DOMINANT 3; PEOA3 description, symptoms and ... Progressive External Ophthalmoplegia Evaluation (POLG, TWINKLE, ANT1, OPA1, MELAS). By Athena Diagnostics Inc (United States). ... Progressive External Ophthalmoplegia With Mitochondrial Dna Deletions, Autosomal Dominant 3; Peoa3. Table of contents: * ... Progressive External Ophthalmoplegia With Mitochondrial Dna Deletions, Autosomal Dominant 3; Peoa3 Recommended genes panels. ...
Complete Ophthalmoplegia as a Complication of Acute corticosteroid- and pancuronium- associated myopathy. In: Neurology. 1991 ... Complete Ophthalmoplegia as a Complication of Acute corticosteroid- and pancuronium- associated myopathy. / Sitwell, Lucian D ... abstract = "We report acute complete external ophthalmoplegia and severe myopathy in a patient treated with high doses of IV ... N2 - We report acute complete external ophthalmoplegia and severe myopathy in a patient treated with high doses of IV ...
ophthalmoplegia. ophthalmoplegia, paralysis of the extraocular muscles that control the movements of the eye. Ophthalmoplegia ...
Cavernous sinus thrombosis (CST) was initially described by Bright in 1831 as a complication of epidural and subdural infections. The dural sinuses are grouped into the sagittal, lateral (including the transverse, sigmoid, and petrosal sinuses), and cavernous sinuses.
Learn about oscillopsia, including conditions that may cause it to occur.
Download Chronic Progressive External Ophthalmoplegia (CPEO) Chyle Leak; Fat free diet for a chyle leak. *Area of Care: ... Chronic Progressive External Ophthalmoplegia (CPEO). *Area of Care: Ophthalmology. *Tags: 6205, ataxia, disease, dysphagia, ...
Ophthalmoplegia. *Visual disturbances. Such adverse effects are uncommon, but delayed treatment might contribute to their ...
This diabetic patient with mucormycosis presented with complete ophthalmoplegia and proptosis. Note the complete ptosis and ...

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