Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The case of a man 34 year-old presenting upward gaze paralyses and external ophthalmoplegia without involvement of the downward gaze, accompanied by cerebellar disorders, generalized areflexia but no muscular weakness, and moderate sensory impairment of the four extremities is reported. The cerebrospinal fluid showed an albuminocytologic dissociation. Recovery was rapid and almost complete, within 3 weeks, remaining minimal paresis of the upward gaze and lateral movement in both eyes. The improvement had been coinciding with the treatment by cortrosina.
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PMID:[Miller Fisher syndrome. Report of a case]. 715 57

A partial deficiency of pyruvate decarboxylase (PDC) was demonstrated in a child with hyperlactatemia and progressive ataxia, bulbar paresis, ophthalmoplegia, and polyneuropathy. Subacute necrotizing encephalomyelopathy (SNE) was found at necropsy. The association of SNE and PDC deficiency has been reported rarely, but a review of the diverse metabolic defects associated with SNE suggests that decreased PDC activity may be the common feature of SNE.
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PMID:Pyruvate decarboxylase deficiency in subacute necrotizing encephalomyelopathy. 724 88

Fifteen patients with internuclear ophthalmoplegia (INO) were examined by simultaneous electro-oculography of each eye. In 11 patients the INO was bilateral and in 4 patients unilateral. In 6 of the bilateral cases, the INO was asymmetric. A classic presentation of the INO was shown by only 2 patients. The rest had additional disorders of eye mobility (INO plus). The high percentage of additional affections, which were not often clinically apparent, consisted of slowing of abduction (45%), impairment of vertical movements (80%) and convergence (30%), and dysmetric overshoot of the abducing eye (65%). Impairment of vertical movements were combined in 3 patients with unilateral INO. Isolated downward vertical gaze paresis was found in 4 patients. Thus an investigation by quantitative methods demonstrates the very rare occurrence of isolated lesions of the medial longitudinal fascicle (MLF). Affections of the MLF mostly are combined with lesions of the surrounding reticular formation and therefore with additional optomotoric defects.
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PMID:[Internuclear ophthalmoplegia and associated oculomotor syndrome (author's transl)]. 725 80

The case of a patient with paralysis of the lateral gaze to the left, paresis of both eyes when he tried to look upwards and a disfunction of the cerebellum to the left, is reported. During the evolution the paresia of both eyes when the patient looked upwards and the disfunction of the cerebellum disappeared, but the paralysis of the lateral gaze to the left, remained. Later on the patient went a little confuse, did not understand what other persons spoke to him, and speak badly. The necropsy showed one old infarct in the medial longitudinal fasciculus in the left, the same type of lesion in the ventral part of the upper pons which was also to the left and demyelinization of the motor lemniscus of the same side. It was also seen a more recent infarct in the transverse gyrus of the left cerebral hemisphere and also the white matter below it. The study of the medial longitudinal fasciculus by means of the secondary degeneration showed that it was crossed above the 6 degrees nuclei, but was straight to the contrary of what is said about it. The authors also observe that the cells of the interstitial nucleus of Cajal were in chromatolysis. These findings justify the syndrome and the absence of the internuclear anterior ophthalmoplegia to the right.
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PMID:[Paralysis of the conjugated lateral gaze of pontile origin: neuroanatomical discussion of the fasciculus longitudinalis medialis]. 725 93

An unclassified type of ophthalmoplegia, composed of sixth-nerve paresis and Horner's syndrome without facial anhidrosis, was studied in an 18-year-old woman following cranial trauma. Carotid angiography disclosed a traumatic intracavernous carotid aneurysm. According to previous anatomical reports, an important sympathetic nerve joins the sixth cranial nerve in the posterior part of the cavernous sinus. An expansive process into the cavernous sinus at this point may cause this unclassified neurological syndrome. A review of the literature and a detailed clinical study were made.
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PMID:An unrecognized neurological syndrome: sixth-nerve palsy and Horner's syndrome due to traumatic intracavernous carotid aneurysm. 728 Sep 87

High resolution infra-red oculographic recordings were obtained in 19 patients with clinically evident internuclear ophthalmoplegia. The major findings were attenuated phasic and tonic components of adducting saccades, fractionated phasic components of abducting saccades, equally long durations for phasic components of adducting and abducting saccades with refixation, and nasal drift of the abducting eye which initiated abducting nystagmus. Ipsilateral gaze paresis and abduction lag were occasionally associated with primarily unilateral cases of internuclear ophthalmoplegia. These findings were interpreted using available anatomical, electromyographic and oculographic data as well as computer simulations of internuclear ophthalmoplegia. We concluded that deficient excitation of the ipsilateral medial rectus was due to interruption of burst-tonic neurons within the medial longitudinal fasciculus which mediate horizontal eye movements. This resulted in a decreased pulse height and step of the agonist neural controller signal. We were also able to determine that variably slowed fractionated abducting saccades were caused by deficient intrasaccadic inhibition of the antagonist medial rectus. When medial rectus excitation was more deficient than medial rectus inhibition of the opposite eye, then a typical internuclear ophthalmoplegia resulted; when the amount of medial rectus excitation was equal to the amount of medial rectus inhibition of the opposite eye, then a gaze paresis occurred; and when medial rectus excitation was less deficiennt than medial rectus inhibition of the opposite eye, abduction lag resulted in the oculographic appearance of internuclear ophthalmoplegia of abduction. Abducting nystagmus appeared to be initiated by a tendency for the abducted eye to drift nasally from the increased level of tonic inhibition of the antagonist medial rectus. Some oculographic patterns were attributed to higher level adaptive changes in innervation. These changes were a consequence of disordered excitatory and inhibitory controller signals at the lower, internuclear level. Possible anatomical pathways which might carry these inhibitory controller signals were discussed. High resolution eye movement recordings of patients with internuclear ophthalmoplegia were interpreted directly and by computer simulations as being most consistent with disordered inhibitory and excitatory control of the medial rectus motor pool during rapid eye movements and eccentric gaze.
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PMID:Disordered inhibition in internuclear ophthalmoplegia: analysis of eye movement recordings with computer simulations. 736 56

A 57-year-old woman developed pain behind and above her left eye. She had a partial oculomotor nerve paresis manifest by slight blepharoptosis and a dilated pupil. Both anterior chamber angles were narrow but the left was partially occluded. There was no photophobia or corneal edema. Though the moderately increased intraocular pressure was controlled by medication, pain persisted and the oculomotor nerve palsy became complete 12 hours later. Cerebral angiography was done. She had an aneurysm of the left posterior communicating artery. The aneurysm was treated by neurosurgical techniques and the oculomotor paralysis resolved within a few months except for misdirection in regeneration.
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PMID:Acute angle-closure glaucoma secondary to an aneurysm of the posterior communicating artery. 738 66

In 1964, a 51-year-old man experienced a right abducens nerve palsy, which resolved spontaneously. In 1978, he developed painful ophthalmoplegia on the right with paresis of the right oculomotor and trigeminal nerves. Neuroradiographic evaluation was reported unremarkable, and the painful ophthalmoplegia was attributed to the Tolosa-Hunt syndrome. High-dose corticosteroids were administered with transient improvement of signs and symptoms. In 1979, cranial computerized tomography demonstrated a low-density lesion adjacent to the right cavernous sinus, which at operation proved to be an epidermoid tumor.
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PMID:Parasellar epidermoid tumor presenting as painful ophthalmoplegia. 746 10

Three of 22 patients (14%) who underwent anterior temporal lobectomy for treatment of medically intractable epilepsy at our institution from July 1987 through July 1993 experienced diplopia immediately after surgery. We found ipsilateral paresis of the superior oblique muscle in all three patients. Their ophthalmoplegia resolved completely within 14 weeks. We did not observe any new structural or ischemic changes on postoperative MRIs to account for their deficits. Trochlear nerve palsy--not oculomotor nerve palsy, as is reported in most reference texts--is a relatively common cause of transient diplopia following temporal lobectomy. Indirect (ie, traction) injury of the trochlear nerve is a plausible mechanism that would explain this complication.
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PMID:Transient trochlear nerve palsy following anterior temporal lobectomy for epilepsy. 764 42

A 49-year-old man who had been suffering from poorly controlled diabetes mellitus for 20 years was admitted to our hospital with the chief complaints of diplopia and right ptosis. The onset of his symptoms was sudden. On admission, he had right palpebral ptosis, upward and left lateral gaze paresis of the right eye. Hess screen chart examination revealed paresis of the right superior rectus, inferior oblique and medial rectus muscles. T2 weighted magnetic resonance imaging (MRI) revealed high intensity area in the medial part of the right midbrain tegmentum where the oculomotor nucleus located, and diffusion weighted MRI demonstrated high intensity area which corresponded to the oculomotor fascicles of the midbrain. The latter represented Wallerian degeneration of the fascicles. The diagnosis of small infarction of the right oculomotor nucleus presenting ipsilateral external ophthalmoplegia was made. The superior rectus muscle is innervated by the neurons in the contralateral oculomotor nucleus, and the other external ocular muscles innervated by the third cranial nerve are conducted by the neurons in the ipsilateral oculomotor nucleus; therefore, unilateral oculomotor nuclear lesion generally causes ipsilateral ophthalmoplegia plus contralateral superior rectus palsy. Our case presented here shows that there may be such a case with oculomotor nuclear disturbance which masquerades with oculomotor fascicular or infranuclear disturbance; therefore, it is important to include these lesions in differential diagnosis.
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PMID:[Unilateral external ophthalmoplegia caused by ipsilateral oculomotor nuclear lesion: analysis with diffusion weighted MRI]. 782 Sep 68


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