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)

The authors begin by enumerating the various syndromes in which painful ophthalmoplegia may be observed (sphenoidal fissure syndrome, Collier's syndrome, syndromes involving the orbital apex, the cavernous sinus and parasellar syndromes; Raeder's syndrome, Gradenigo's syndrome and Fischer-Brugge syndrome). They then discuss the various causes that must be investigated in all cases of painful ophtalmoplegia. They consider in order: -- ophtalmoplegia due to general causes (especially diabetes) and neurological causes (e.g. multiple sclerosis); -- ophtalmoplegia due to common local canses space-occupying processes, vascular malformations, ear, nose and larynx infections); -- painful ophalmoplegia of unknown origin, which includes four entities of very differing importance (Gubler and Charcot's ophthalmoplegic migraine and Tolosa-Hunt syndrome of which the clinical symptoms and course are so different that they can be distinguished as two entities; and, secondarily, inflammatory pseudo-tumours of the orbit and the recurrent multiple cranial nerve palsies that are observed in South-East Asia). (Acta nurol. belg., 1977, 77, 331-350).
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PMID:[Painful ophthalmoplegia (author's transl)]. 2 45

The early components of the auditory evoked responses (waves I-V) have been studied in 30 patients with multiple sclerosis. There were abnormalities in 22 patients. All patients with an internuclear ophthalmoplegia and half those with no detectable brainstem abnormality had abnormal responses, although none was clinically deaf.
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PMID:Auditory evoked responses in multiple sclerosis. 4 77

Whipple's disease presenting as a neurological disease without gastrointestinal symptoms is an unusual occurrence. A 40 year old man suffered hypersomnia, memory loss and progressive ophthalmoplegia for 6 months prior to death. The nature of this disease was not established during life. Extensive granulomatous inflammation affecting the hypothalamus, hippocampus and periaqueductal gray matter of the brain was found to represent Whipple's disease by electron microscopy. Characteristic lesions were also present in spleen, mesenteric lymph nodes, small intestine and myocardium. Bacillary bodies and membranous inclusions similar to those seen in visceral lesions of Whipple's disease were present in macrophages. The findings supported the theory of direct involvement of the central nervous system by bacilli rather than a metabolic origin for the lesions.
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PMID:Whipple's disease of the central nervous system. 6 98

4 patients are described with ophthalmoplegia (Figs. 1 and 2) and ataxia with acute onset. Three of them showed only very slight symptoms of generalized polyneuritis. Measurement of sensory nerve conduction velocity (Fig. 4, Table 2) and determination of vibration sense by an electrical vibrator (Fig. 3) proved to be helpful for diagnosis. The ocular EMG revealed signs of peripheral denervation in 3 cases. Pathological changes of the somatosensory evoked potential (Fig. 5) which has been registered in one case, might give some speculation as to whether or not central nervous pathways are affected.
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PMID:Electrophysiological findings in the syndrome of acute ocular muscle palsy with ataxia (Fisher syndrome). 6 26

Four patients with Whipple's disease which had responded to antibiotic therapy, later developed neurologic disease identical to that seen in patients with Whipple's disease who died without treatment. Dementia, myoclonus, ataxia, and supranuclear ophthalmoplegia were the main neurologic features. Restarting antibiotics has been followed by stabilization of disease in all four. Two have improved. In three, the previously diagnosed and treated Whipple's disease was not considered as a possible cause of the neurologic disease until the symptoms and signs were far advanced. It is advisable to periodically evaluate all patients with Whipple's disease, even after successful treatment. Signs of neurologic disease should be considered a possible recurrence of Whipple's disease and antibiotics restarted.
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PMID:Neurologic disease in patients with treated Whipple's disease. 6 1

Head movement-dependent oscillopsia (HMDO) with peripheral vestibular, brainstem and cerebellar lesions is reviewed. The differentiation of this kind of oscillopsia is based mainly on clinical grounds. HMDO with bilateral abolition of caloric responses, and in the absence of disease of the central nervous system, is due to bilateral vestibular disease. HMDO in patients with internuclear ophthalmoplegia and other brainstem signs is probably due to a lesion of VOR pathways in or near the medial longitudinal fasciculus. The occurrence of HMDO with ataxia of gait and cerebellar eye movement disorders (rebound nystagmus, flutter-like oscillations), in the absence of brainstem lesions (medial longitudinal fasciculus), is clinical evidence for HMDO due to a cerebellar lesion. An attempt is made to associate the different kinds of oscillopsia with current knowledge of the vestibulo-ocular reflexes.
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PMID:Clinical and theoretical aspects of head movement dependent oscillopsia (HMDO). A review. 8 58

A case of progressive extrinsic ophthalmoplegia associated with peripheral neuropathy and hypertriglyceridemia type IV is described. Motor and sensory conduction velocities of the spinal nerves were severely decreased, while the EMG of the facial muscles was more suggested of a myopathic disorder. Electron microscopic study of biopsies of biceps and peroneus brevis muscles disclosed many ragged red fibers, mainly type I, which contained typical abnormal mitochondria. Other fibers, all type II, contained increased amounts of glycogen between myofibrils or beneath the sarcolemmal membrane, but the mitochondria were normal. These fibers were more abundant in the peroneus brevis than in the biceps muscle. Nerve biopsy revealed marked loss of myelinated fibers, but neither mitochondrial changes nor glycogen storages were evident in Schwann's cells. Biochemical investigations confirmed the increased amount of glycogen in both muscle biopsies and revealed a decrease of guanilcyclase. Phosphorylase, phosphorylase b kinase, adenilcyclase, and carnitine concentrations were all normal. The pathogenesis of this syndrome is discussed and the relationship between mitochondrial abnormalities and glycogen accumulation in muscle tissue are considered.
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PMID:Progressive extrinsic ophthalmoplegia with peripheral neuropathy and storage of muscle glycogen. 9 34

A case of Whipple's disease with central nervous system (CNS) involvement has been retrospectively diagnosed. At the age of 50 and after six years of recurrent bouts of pyrexia, anorexia and loss of weight, a man developed a subacute encephalitis. Two episodes of acute loss of vision were followed by changes in mental status, supranuclear ophthalmoplegia and oculo-facio-cervical myorhythmias which remained present until death, one year later. Combined light- and electron microscopic studies have demonstrated: No. 1 the presence in the CNS of nodules containing large amounts of Sieracki cells; No. 2 the existence of bacteria in various stages of degeneration in macrophages or in the neuropile. A review of CNS complications in Whipple's disease is made.
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PMID:Cerebral manifestations of Whipple's disease. 9 79

Twenty-six patients with painful ophthalmoplegia were classified as having the Tolosa-Hunt syndrome on the basis of their clinical findings and response to steroid therapy. All patients underwent orbital venography, a review of which forms the contents of this investigation. Orbital venography, a review of which forms the contents of this investigation. Orbital venograms were normal in 16 patients and abnormal in 10. The major abnormalities were (1) obstruction of the superior ophthalmic vein in its third segment without displacement; (2) collateral venous flow through small venous channels or collateral veins; and (3) poor opacification of the ipsilateral cavernous sinus.
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PMID:Orbital venography in painful ophthalmoplegia (Tolosa-Hunt syndrome). 11 66

Three cases of Kearns syndrome are reported. The neuro-ophthalmological signs were comparable with ophthalmoplegia, pigmentary retinal degeneration and polymorphic neuro-muscular and sensory deficits. The electrocardiological signs were observed 2-4 years after the onset of the condition; the cause of death in each case was related to complete heart block. The post-mortem findings in one of the cases were spongial degeneration of the central nervous system and a seemingly primitive degeneration of the Bundle of His and its branches.
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PMID:[Cardiological aspect of Kearns' syndrome. Apropos of 3 cases, with histopathological study of the conduction tissue in one of them]. 11 5


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