Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029089 (ophthalmoplegia)
 3,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 17-year old girl received prednisone and azathioprine for the treatment of systemic lupus erythematosus. She developed a fever and hallucinations 18 months later; cryptococcal meningitis was diagnosed. An internal ophthalmoplegia with loss of accommodation and dilation of the pupils developed together with bilateral lateral rectus palsy. Treatment with intravenous amphotericin resulted in disappearance of papilledema, muscle palsy, and internal ophthalmoplegia. We believe that the internal ophthalmoplegia was secondary to involvement of the accommodative and pupillary fibers of both third nerves at the base of the brain.
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PMID:Cryptococcal meningitis and internal ophthalmoplegia. 44 40

A patient is described who simultaneously suffered from hallucinations and one-and-a-half syndrome following surgical resection of a cavernous angioma located on the fourth ventricle floor. A 30-year-old male was admitted having a 10 year history of progressive weakness and hypesthesia of the right extremities. Neurological examination revealed right hemiparesis and hemihypesthesia. A computerized tomography (CT) scan showed a well circumscribed mixed-density area at the left portion of the pontine tegmentum. Magnetic resonance imaging (MRI) indicated a mixed intensity core surrounded by hypointense regions on T2-weighted images. A red mulberry-like tumor was found, during surgical procedures, on the mid-and left-portion of the fourth ventricle floor. The tumor was totally resected and the histological diagnosis was cavernous angioma. Visual hallucinations occurred several times following surgery, being subsequently described as images of moving worms, a dump truck next to the bed, and a bed falling from the ceiling. The patient soon understood these objects were not real. He simultaneously exhibited left lateral gaze palsy associated with left internuclear ophthalmoplegia i.e., one-and-a-half syndrome. Three months after surgery the visual hallucinations disappeared but the one-and-a-half syndrome was incompletely resolved. According to the neurological signs and the MRI results, the lesion site was considered to extend from the left lower pons to the midbrain. Previously reported operations of cavernous angioma of the fourth ventricle floor are also described.
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PMID:[Appearance of hallucinations and one-and-a-half syndrome after resection of a cavernous angioma located in the fourth ventricle floor]. 845 3

Diplopia, nystagmus, visual hallucinations, and internuclear ophthalmoplegia developed in a 30-year-old woman 84 days after she received a matched, unrelated bone marrow transplant for chronic myeloid leukemia. A regimen of tacrolimus had been administered since the transplantation was performed. MR imaging revealed bilaterally symmetric regions of signal abnormality with abnormal contrast enhancement in the brain stem. No supratentorial abnormality was present. Tacrolimus therapy was discontinued, and the symptoms resolved. MR imaging that was performed 10 days after tacrolimus was discontinued showed resolution of the abnormalities.
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PMID:Reversible tacrolimus-induced neurotoxicity isolated to the brain stem. 1095 77

The Kearns-Sayre syndrome (characterized by onset before 20, chronic ophthalmoplegia, pigmentary retinal degeneration and at least 1 of the following symptoms: ataxia, heart block and high protein content in the cerebrospinal fluid) is a severe variant of chronic progressive external ophthalmoplegia (CPEO) with frequent re-arrangements of the mitochondrial DNA (mtDNA). The aim of this paper is to report a sporadic paediatric case of Kearns-Sayre syndrome with mtDNA heteroplasmic deletion, absence of cytochrome c oxidase in many muscle fibers, autoimmune thyroiditis followed by depressive phobic disturbances, slowing EEG, hyperreflexia, tremor and visual hallucinations, in which the diagnosis of possible encephalopathy associated with autoimmune thyroid disease (Hashimoto encephalopathy) was made. We speculated that in this patient, predisposed by mitochondrial deletion, anti-thyroid antibodies may have interfered with mitochondrial cerebral function, causing Hashimoto encephalopathy and facilitating ophthalmoplegia. It seems important to study anti-thyroid antibodies in every case of Kearns-Sayre syndrome, specially if ophthalmoplegia is recent, even in order to the therapy.
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PMID:A case of Kearns-Sayre syndrome with autoimmune thyroiditis and possible Hashimoto encephalopathy. 1209 44

Vertigo can be defined as an illusion or hallucination of movement. The control of balance is complicated. Vertigo can be caused by many different pathologies, some of which are potentially life threatening. An important differentiation is whether the symptoms of vertigo originate from a central or peripheral origin. Clues to a central origin are other brainstem symptoms or signs of acute onset such as headache, deafness and other neurological findings. These patients warrant urgent referral and investigation. Red flags in patients with vertigo include: headache; neurological symptoms; and neurological signs. It is useful to categorise vertigo into acute and chronic. The former usually has a single mechanism whereas chronic dizziness is often multifactorial. History is usually the most important part of the assessment. Key questions should be asked and it is vital to establish if the patient is suffering from vertigo or some other complaint such as anxiety or syncope. A neurological and otological examination should be performed, appropriate to the history. Assessment of gait and posture is crucial. If the patient has positional vertigo then a Hallpike test should be performed. Visual acuity should be checked as vision is a vital part of the balance system. The cranial nerves should be tested in particular eye movements for any ophthalmoplegia pointing to focal cranial nerve pathology and for nystagmus. The rest of the neurological examination should exclude evidence of central disease, in particular cerebellar disease, and neuropathy. If syncope is suspected it is wise to perform an extensive systemic examination in particular lying and standing BP, and cardiovascular and respiratory system assessments.
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PMID:Systematic approach needed to establish cause of vertigo. 2151 May 8

A 40-year-old man presented with respiratory compromise and was intubated. After tracheostomy, he was found to have ophthalmoplegia, severe limb rigidity, stimulus-sensitive myoclonus and autonomic dysfunction. For 1 week before admission, there had been a prodromal illness with low mood, hallucinations and limb myoclonus. Serum glycine receptor antibodies were strongly positive: we diagnosed progressive encephalomyelitis with rigidity and myoclonus. Despite a relapse, he has done well following immunotherapies. The clinical syndrome of encephalomyelitis with rigidity, described in 1976, often has a severe progressive course. A minority of patients have glutamic acid decarboxylase antibodies. The association with glycine receptor antibody was first reported in 2008, and we briefly review subsequent case reports to illustrate the range of clinical features. The antibody is likely to be disease mediating, although this remains unproven. The spectrum of diagnosable and treatable antibody mediated neurological syndromes is expanding. It is vital to recognise these conditions early to reduce morbidity and mortality.
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PMID:Glycine receptor antibody mediated Progressive Encephalomyelitis with Rigidity and Myoclonus (PERM): a rare but treatable neurological syndrome. 2356 94

We herein report the case of a 26-year-old woman with anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis presenting with ophthalmoplegia and flaccid paraplegia. She developed disorientation and hallucination after fever and vomiting. Hypothermia, hypoventilation, hypertension, paralytic ileus and hyponatremia were present. Neurological examination showed mild consciousness disturbance and bilateral ophthalmoplegia on admission, flaccid paraplegia with leg areflexia on Day 4. Anti-NMDAR antibodies were detected in the serum and cerebrospinal fluid samples. Motor nerve conduction velocity was decreased in the tibial and peroneal nerves. F-wave amplitudes were reduced in the tibial nerve. MRI disclosed lesions in the callosal splenium, hippocampus and cerebral subarachnoid regions. In addition to various encephalitic symptoms, physicians should pay more attention to peripheral nerve damage in patients with anti-NMDAR encephalitis.
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PMID:Ophthalmoplegia and flaccid paraplegia in a patient with anti-NMDA receptor encephalitis: a case report and literature review. 2433 91