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)

Tolosa Hunt syndrome is a rare disorder caused by nonspecific inflammation in the cavernous sinus/superior orbital fissure and/or orbital apex. It is clinically characterized by alternating remissions and exacerbations, and manifested as diplopia associated with unilateral periorbital hemicranial headache. The symptoms include blepharoptosis, which is usually mild if present, bulbomotor paresis involving the pupil, and loss of sensation in the area supplied by the first division of the trigeminal nerve. Therapy for Tolosa-Hunt syndrome are systemic steroids. The course of disease in a 25-year-old man hospitalized for painful ophthalmoplegia and diplopia is presented. The history included severe pain on rightward eye movement and parabulbarly on the right, considerable defect in the area supplied by the first division of the trigeminal nerve, right hemicrania, and diplopia on looking to the left, right, upward and downward that developed after four days. A month before, the patient was observed at neurology department for severe right hemicrania. Current status included severe pain parabulbarly on the right, discrete proptosis with mild ptosis on the right eye, restricted right eye bulbar motoricity on looking nasally, nasally upward and downward, and loss of sensation in the area supplied by the first division of the trigeminal nerve. Pupilar motoricity was normal. Upon admission, neuroradiologic examination (orbit CT) and brain MR were performed, and therapy with systemic corticosteroids was initiated ex iuvantibus, in consultation with a neurologist. At 24 hours of corticosteroid therapy, the pain subsided, whereas diplopia disappeared almost completely after 5 days, now being only occasionally recorded on looking to the left and upward.
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PMID:[Painful ophthalmoplegia--Tolosa-Hunt syndrome]. 1804 75

Horner's syndrome, or oculosympathetic paresis, results from interruption of the sympathetic trunk innervation to the eye and presents typically with meiosis, ptosis and facial anhydrosis on the affected side.(1) The pathological process ranges from benign, such as cluster headache, or life threatening, such as lung malignancy. Appropriate imaging requires an anatomical appreciation of the complex and circuitous route the neuronal pathway takes as it passes from the central nervous system to the eye.
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PMID:Imaging of Horner's syndrome. 1837 11

This case describes a patient who developed a complete right hemiparesis with ptosis of eyelid, trigeminus and facial paresis following a routine epidural analgesia for labor. A subdural deposit of the local anaesthetic might be the cause of these symptoms. The pathogenesis of these symptoms as well as the diagnoses and treatment of the condition is discussed.
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PMID:[A rare complication of labor epidural analgesia]. 1856 19

A 27-year-old man presented with a 2-month history of retro-orbital pain and a 2-week history of progressive ptosis and diplopia. Neurological examination revealed left partial third, fourth and sixth cranial nerve paresis. Imaging revealed a large middle fossa lesion with heterogeneous signal intensity. During surgery, the tumor was found to be entirely within the confines of the dural layers of the lateral wall of the cavernous sinus. Histological analysis revealed that the tumor was a mature teratoma. The case is discussed and the literature on this rare location of teratoma is reviewed.
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PMID:Giant interdural teratoma of the cavernous sinus. 1884 10

A 45-year-old female developed mild dysesthesia and swelling, followed by ptosisand trigeminal pain, in the right side of the face. Her past medical history was unremarkable, and she had not been aware of any infectious sign. A local otolaryngologist administered glucocorticoid therapy that resolved the face pain, but the ptosis persisted. Neurological examination found complete right oculomotor nerve paresis and mild sensory loss in the first and second segments of the right trigeminal nerve. Blood examination found no abnormalities. Neuroimaging revealed a saccular aneurysm at the branching site of the posterior communicating artery, projecting posteriorly and adjacent to the dorsum sellae, without other intracranial abnormalities. Cerebral angiography demonstrated poor opacification of the superior ophthalmic vein and cavernous sinus on the right side. The patient underwent coil embolization under a diagnosis of symptomatic aneurysm, but her oculomotor neuropathy was only partially improved. We thought that the impairment of the oculomotor function by inflammatory reaction in the cavernous sinus and mechanical compression by the aneurysm had already persisted for too long for post-treatment recovery. We think that the simultaneous occurrence of Tolosa-Hunt syndrome and oculomotor nerve palsy may have resulted because trigeminal neuralgia had increased the blood pressure to induce rapid growth of the preexisting aneurysm, or the inflammatory reaction in the cavernous sinus had promoted the growth of the aneurysm, or that the association was by chance.
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PMID:[Simultaneous presentation of Tolosa-Hunt syndrome and oculomotor nerve palsy due to the nonruptured internal carotid-posterior communicating artery aneurysm: a case report]. 1936 32

We report a patient who has a tremor and unilateral ptosis and mydriasis without extraocular muscle paresis from an intra-axial lesion demonstrated on neuroimaging. Previously extraocular muscles sparing partial third nerve palsy has been thought to be due to extra-axial lesion such as vascular compression. Compared to proposed models for arrangement of oculomotor fascicle, this case demonstrates that it is possible to damage the fibers destined for levator and pupillomotor function without affecting the extra-ocular muscles.
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PMID:Isolated unilateral ptosis and mydriasis from ventral midbrain infarction. 1939 Jul 69

Tolosa-Hunt syndrome (THS) is characterized by unilateral painful ophthalmoplegia with oculomotor paresis, associated with an idiopathic granulomatous inflammation involving the cavernous sinus, with a typical relapsing-remitting course. We report a case of an 8-year-old girl who was admitted because of an ophthalmoplegia with exotropia and ptosis of the left eyelid, accompanied by diplopia and left sovraorbital pain. The clinical data, neuroradiological findings and response to steroid treatment suggested THS, as defined by the 2004 International Classification of Headache Disorders (ICHD)-II criteria. THS must be considered a possible cause of painful ophthalmoplegia in childhood, as well as in adults, and confirmed with a focused neuroradiological investigation. The few paediatric cases described in the literature that meet the 2004 ICHD-II criteria are not sufficient to identify possible differences between the paediatric and the adult forms. Every new paediatric case should therefore be reported in order to gather and compare further information.
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PMID:The Tolosa-Hunt syndrome in children: a case report. 1955 37

Transient affliction of the cranial nerves may at times be either the presenting feature or complication of otherwise uncomplicated Kawasaki disease (KD) in infants and children. The present report describes a 6 year 9 month old boy with classical KD who developed right-sided oculomotor nerve palsy (manifested by ipsilateral ptosis and medial rectus palsy) resulting in symptoms like severe nausea, intense frontal headache and double vision. The palsy resolved within 5 days of intravenous immunoglobulin therapy, with no residual ophthalmological abnormality at 6 weeks. Besides increased intracranial pressure, which commonly occurs during the course of KD in children, secondary to aseptic meningitis, intense headache in such children may have cranial nerve paresis as accentuating factors.
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PMID:Transient unilateral oculomotor palsy and severe headache in childhood Kawasaki disease. 1982 42

Headache associated with moyamoya disease (HAMD) is common in moyamoya disease. However, the characteristics and classification of HAMD are largely unknown. We present a case of a 39-year-old woman with HAMD. To characterize and classify the features of this syndrome, the patient was asked to complete a 4-month diagnostic headache diary. There was a total of 15 ictal days. All episodes were without aura. The headache was more commonly pressing (10/15), mild to moderate in severity (14/15), unchanged by physical activity (11/15), and associated with photophobia (10/15). The International Headache Society Classification was utilized to determine that eight episodes met criteria for probable migraine without aura, while seven episodes met criteria for probable frequent episodic tension-type headache. We identified four other case reports of HAMD with partial descriptions of the characteristics. When combined with our patient, the median age was 34 years old (range 6-49, SD 16). Four were female, while the patient with cluster headache was male. The median time from headache onset to diagnosis with moyamoya disease was 9.5 months (range 0-192, SD 88.0). Headaches were described as migraine with aura in two of five cases, hemiplegic migraine in one of five, and cluster headache in one of five. The highest intensity was described as severe in three of three cases, in which headache intensity was reported. Meanwhile, nausea, vomiting, and photophobia were present in two of three cases, where these features were reported, while nausea without vomiting was seen in one of three cases. In all five cases, patients had other neurological symptoms, such as paresis, seizures, visual disturbances, dysarthria, allodynia, ptosis, and unilateral restless leg syndrome. In conclusion, HAMD can present as migraine without aura. It can be the first presenting symptom of moyamoya disease. The headache features are not diagnostic; hence, early neurovascular imaging should be considered in patients with new onset, refractory migraine-like headache, especially in the setting of other neurological symptoms to exclude underlying moyamoya disease. Further reports using headache diaries are needed to better characterize HAMD as well as to determine whether headache with tension-type features is also part of this condition.
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PMID:Headache associated with moyamoya disease: a case story and literature review. 2001 51

We treated a patient who developed binocular diplopia and ptosis after being bitten by an Agkistrodon blomhoffi (mamushi). The patient was a 49-year-old man who presented with binocular diplopia after the snakebite on the second finger of his right hand. He experienced local pain and swelling and a few hours later, he developed diplopia. In the primary position he had no tropia. On the basis the ocular angle of deviation measured by a Hess chart test, he was diagnosed with paresis of the medial rectus muscle paresis. Binocular diplopia persisted for 2 weeks. The venom of A. blomhoffi venom mainly consists of hemolytic toxins, but it also contains 2 types of neurotoxins--an alpha-toxin and a beta-toxin. Neurotoxins affects the neuromuscular junction (NMJ). The alpha-toxin acts postsynaptic inhibition as a competitive inhibitor of acetylcholine and causes postsynaptic inhibition; these effects are similar to those of the anti-acetylcholine receptor antibody identified in patients with myasthenia gravis. The beta-toxin inhibits acetylcholine release by disrupting the presynaptic membrane, and thus, its effects cannot be blocked by the anticholinesterase edrophonium chloride. Although both antiserum and cepharanthine are widely used for the treatment of snakebites, there is no evidence of a specific effective therapy for the eye manifestation after snakebite. However, it these manifestation improves in about 2 weeks without any specific treatment. Our case suggested that the occurrence of subjective binocular diplopia without objective tropia could be caused by snakebite.
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PMID:[Binocular diplopia and ptosis due to snakebite (Agkistrodon blomhoffi "mamushi")--a case report]. 2029 33


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