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1 sis that sometimes evolved to total external ophthalmoplegia.
2  neuropathy and chronic progressive external ophthalmoplegia.
3 half of the subjects studied had evidence of ophthalmoplegia.
4 rum levels of creatine kinase and a profound ophthalmoplegia.
5 osis and a restrictive infraductive external ophthalmoplegia.
6 ented with myopathy and progressive external ophthalmoplegia.
7 ssary for good clinical outcomes in cases of ophthalmoplegia.
8 myopathy and late-onset progressive external ophthalmoplegia.
9 eroid led to complete resolution of external ophthalmoplegia.
10 tochondrial disease and progressive external ophthalmoplegia.
11 defect in patients with progressive external ophthalmoplegia.
12 polymerase, is typically proximal with early ophthalmoplegia.
13 Alpers syndrome to mild progressive external ophthalmoplegia.
14 lowed by development of progressive external ophthalmoplegia.
15  as Alpers syndrome and progressive external ophthalmoplegia.
16 nd generalized limb weakness with ptosis and ophthalmoplegia.
17 d with certain types of progressive external ophthalmoplegia.
18  for autosomal dominant progressive external ophthalmoplegia.
19 onism in the absence of progressive external ophthalmoplegia.
20 ittle or no facial weakness or ptosis and no ophthalmoplegia.
21 py eyelids (ptosis) and progressive external ophthalmoplegia.
22  and autosomal dominant progressive external ophthalmoplegia.
23 py eyelids (ptosis) and progressive external ophthalmoplegia.
24 roptosis, limited supraduction, and variable ophthalmoplegia.
25 udies have supported the use of internuclear ophthalmoplegia, a model to study effects of fatigue and
26                                 Internuclear ophthalmoplegia, a new finding, was present in two of ou
27 ause autosomal dominant progressive external ophthalmoplegia (adPEO) with multiple mtDNA deletions (M
28 ause autosomal dominant progressive external ophthalmoplegia (adPEO), cardiomyopathy, and myopathy.
29 ause autosomal dominant Progressive External Ophthalmoplegia (adPEO), mitochondrial myopathy and card
30 omes (MDS) and familial progressive external ophthalmoplegia (AdPEO).
31 ar-old man presenting with left-sided, total ophthalmoplegia after a traffic accident.
32  often include severe headache, visual loss, ophthalmoplegia, altered consciousness, and impaired pit
33 alence and important risk factors related to ophthalmoplegia among diabetic patients.
34 data on the epidemiology and risk factors of ophthalmoplegia among diabetic patients.
35 h genetic disorders such as chronic external ophthalmoplegia and Alpers syndrome.
36 nts have been linked to progressive external ophthalmoplegia and ataxia neuropathies among other mito
37 rders including Alpers, progressive external ophthalmoplegia and ataxia-neuropathy syndrome.
38 d children presenting with severe congenital ophthalmoplegia and facial weakness in the setting of on
39                    Clinically, the patients' ophthalmoplegia and facial weakness were far more signif
40  in the differential diagnosis of congenital ophthalmoplegia and facial weakness, even without clinic
41 ross motor regression, hypotonia, ptosis and ophthalmoplegia and had abnormal signals in brainstem an
42 essive muscle weakness, facial dysmorphisms, ophthalmoplegia and intellectual disability.
43 e clinical syndrome characterized by painful ophthalmoplegia and ipsilateral cranial neuropathies.
44  with variable degrees of cerebellar ataxia, ophthalmoplegia and neuropathy.
45 s in multiple sclerosis include internuclear ophthalmoplegia and nystagmus, resulting in diplopia, os
46 biopsy in patients with progressive external ophthalmoplegia and peripheral neuropathy.
47 from dilated cardiomyopathy with adult-onset ophthalmoplegia and progressive skeletal myopathy to a n
48 ion-changing torsional nystagmus, horizontal ophthalmoplegia, and generalized symmetric weakness with
49 pathy characterized by ataxia, areflexia and ophthalmoplegia, and in the majority of cases the presen
50 orders that are characterized by restrictive ophthalmoplegia, and include congenital fibrosis of the
51 mus, autosomal dominant progressive external ophthalmoplegia, and oculopharyngeal muscular dystrophy.
52 ated vertical deviation, sensory strabismus, ophthalmoplegia, and paradoxical diplopia.
53 s contractures of hands and feet, scoliosis, ophthalmoplegia, and ptosis.
54 um; autosomal recessive progressive external ophthalmoplegia; and autosomal dominant progressive exte
55 of Guillain-Barre syndrome, characterized by ophthalmoplegia, areflexia and ataxia.
56 rom 4 families who presented with ptosis and ophthalmoplegia as well as other clinical manifestations
57 nset autosomal-dominant progressive external ophthalmoplegia associated with multiple mitochondrial D
58 G7 are a novel cause of progressive external ophthalmoplegia associated with multiple mitochondrial D
59 gender, family history, progressive external ophthalmoplegia at clinical presentation, hearing loss,
60      Clinically BBE manifests in progressive ophthalmoplegia, ataxia and consciousness disturbances.
61 yndrome (IBS) and anxiety, who presents with ophthalmoplegia, ataxia and memory loss, characteristic
62 subjects from published cases of HZO-related ophthalmoplegia by searching PubMed and Google Scholar,
63                                        Total ophthalmoplegia can result from ryanodine receptor 1 (RY
64 ANTs is associated with progressive external ophthalmoplegia, cardiomyopathy, nonsyndromic intellectu
65                    The overall prevalence of ophthalmoplegia cases was 0.32 %, further distributed in
66 ted by dominant chronic progressive external ophthalmoplegia (CPEO) complicated by parkinsonism and d
67 e a syndrome of chronic progressive external ophthalmoplegia (CPEO) in humans.
68                 Chronic progressive external ophthalmoplegia (CPEO) is common in mitochondrial disord
69 A deletions and chronic progressive external ophthalmoplegia (CPEO) plus syndrome.
70 f mitochondrial chronic progressive external ophthalmoplegia (CPEO)-plus disorders associated with mu
71 red fibers, and chronic progressive external ophthalmoplegia deletion syndromes, with ragged red musc
72  or brainstem syndromes such as internuclear ophthalmoplegia developing over several days.
73 obtaining neuroimaging upon follow-up if the ophthalmoplegia does not improve, progresses, or becomes
74      Autosomal dominant progressive external ophthalmoplegia due to PEO1 mutations is considered rela
75 p of autosomal dominant progressive external ophthalmoplegia due to the p.R357P gene mutation in PEO1
76      Autosomal dominant progressive external ophthalmoplegia due to the p.R357P PEO1 mutation is a la
77 -epilepsy syndrome, and progressive external ophthalmoplegia, each with vastly different clinical pre
78  68 adult patients with progressive external ophthalmoplegia either with or without multiple mitochon
79 roptosis, limited vertical duction, variable ophthalmoplegia, exotropia, and paradoxical abduction in
80 grees in which patients presented with total ophthalmoplegia, facial weakness, and myopathy.
81 ripheral neuropathy and progressive external ophthalmoplegia from the third decade of life onwards.
82 d clinically by ptosis, progressive external ophthalmoplegia, gastrointestinal dysmotility, leukoence
83 ge of 30 years; ptosis; progressive external ophthalmoplegia; gastrointestinal dysmotility; cachexia;
84 patients primarily with progressive external ophthalmoplegia generate T251I and P587L amino acid subs
85 osomal dominant chronic progressive external ophthalmoplegia have been described.
86 ses such as adult-onset progressive external ophthalmoplegia, hepatocerebral syndrome with mtDNA depl
87 a case of herpes zoster ophthalmicus-related ophthalmoplegia (HZORO) in which systemic steroid led to
88  acronym CANOMAD: chronic ataxic neuropathy, ophthalmoplegia, IgM paraprotein, cold agglutinins and d
89          CANOMAD (chronic ataxic neuropathy, ophthalmoplegia, immunoglobulin M [IgM] paraprotein, col
90 he degenerative disease progressive external ophthalmoplegia in humans, and we show that this residue
91 ole of systemic steroids in the treatment of ophthalmoplegia in the setting of herpes zoster ophthalm
92 tended steroid taper may aid the recovery of ophthalmoplegia in the setting of HZO and should be inve
93                Cogan's anterior internuclear ophthalmoplegia (INO) is characterized by INO with inabi
94                   Patients with internuclear ophthalmoplegia (INO) may have preserved vergence, which
95 nted with left Cogan's anterior internuclear ophthalmoplegia (INO), left appendicular ataxia and bila
96        Visual loss from optic neuropathy and ophthalmoplegia involving multiple cranial nerves are th
97 ction 3, in particular, focuses on a form of ophthalmoplegia involving progressive paralysis of extra
98                         Progressive external ophthalmoplegia is a common clinical feature in mitochon
99                                              Ophthalmoplegia is a rare entity associated mainly with
100 g patients with chronic progressive external ophthalmoplegia, Kearns Sayre syndrome, or Pearson's syn
101 uman autosomal dominant progressive external ophthalmoplegia mutations shows differential effects.
102 uman autosomal dominant progressive external ophthalmoplegia mutations.
103 ular dystrophy, chronic progressive external ophthalmoplegia, myotonic dystrophy, neurofibromatosis t
104  retinopathy (n = 1), bilateral internuclear ophthalmoplegia (n = 1), and headache (n = 1).
105 n = 45, 100%), motor weakness (n = 18, 40%), ophthalmoplegia (n = 20, 45%), and bulbar symptoms (n =
106                                              Ophthalmoplegia occurred only when the subarachnoid widt
107                                        While ophthalmoplegia occurs rarely in RYR1-related myopathies
108 smus characterized by congenital restrictive ophthalmoplegia, often with accompanying ptosis.
109 myasthenic manifestations such as ptosis and ophthalmoplegia or facial weakness, and links myasthenic
110 e-Korsakoff syndrome: confusion, ataxia, and ophthalmoplegia or nystagmus.
111  causing infantile mtDNA depletion syndrome, ophthalmoplegia, parkinsonism, male subfertility and, in
112 with autosomal dominant progressive external ophthalmoplegia (PEO) harbour mutations in genes encodin
113                         Progressive external ophthalmoplegia (PEO) is a common feature in adults with
114                         Progressive external ophthalmoplegia (PEO) is a heritable mitochondrial disor
115 s to autosomal dominant progressive external ophthalmoplegia (PEO) with other severe phenotypes.
116 rial diseases including progressive external ophthalmoplegia (PEO), Alpers syndrome and other neuromu
117  recessive and dominant progressive external ophthalmoplegia (PEO), Alpers syndrome, sensory ataxia,
118 pletion syndrome (MDS), progressive external ophthalmoplegia (PEO), ataxia-neuropathy, or mitochondri
119                         Progressive external ophthalmoplegia (PEO), eyelid ptosis, exercise intoleran
120 matopoietic system; and progressive external ophthalmoplegia (PEO), primarily affecting the ocular mu
121 and diabetes (MIDD) and progressive external ophthalmoplegia (PEO).
122 acterized by ptosis and progressive external ophthalmoplegia, peripheral neuropathy, severe gastroint
123 t displayed an indolent progressive external ophthalmoplegia phenotype.
124  results in early onset progressive external ophthalmoplegia, premature ovarian failure, and Parkinso
125 ical symptoms, such as vertical supranuclear ophthalmoplegia, progressive ataxia, and dementia.
126 -adult life with either progressive external ophthalmoplegia/ptosis and spastic ataxia, or a progress
127 e, the genetic basis of progressive external ophthalmoplegia remains unknown in a large proportion of
128 omes such as optic neuritis and internuclear ophthalmoplegia, respectively.
129                                              Ophthalmoplegia secondary to a traumatic dissecting aneu
130 r examination, there was proptosis and total ophthalmoplegia with loss of corneal sensations in the r
131 pol gamma , that causes progressive external ophthalmoplegia with multiple mtDNA deletions and cytoch
132  by a specific form of restrictive paralytic ophthalmoplegia with or without ptosis.
133 mic any pupil-spared, painless, nonproptotic ophthalmoplegia with or without ptosis.
134 al disorders are bilateral optic neuropathy, ophthalmoplegia with ptosis, pigmentary retinopathy, and
135 ed by bilateral ptosis, restrictive external ophthalmoplegia with the eyes partially or completely fi
136 e born with bilateral ptosis and restrictive ophthalmoplegia with the globes "frozen" in extreme abdu

 
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