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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cerebral venous sinus compression can mimic idiopathic intracranial hypertension. The authors report the case of a 12-year-old girl who presented with diplopia and papilledema 3 weeks after a head injury. Lumbar puncture confirmed raised intracranial pressure, and neuroimaging subsequently identified a skull fracture compressing the right transverse sinus. Papilledema and diplopia resolved following surgical elevation of the bone fragment. Computer tomography or magnetic resonance venography are indicated in children presenting with isolated intracranial hypertension following head injury to exclude cerebral venous sinus compression secondary to skull fracture.
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PMID:Isolated intracranial hypertension as a late manifestation of sinus venous compression secondary to a depressed skull fracture. 1762 10

An 88-year-old female with atrial fibrillation and hypertension, was admitted to our hospital with sudden onset diplopia and somnolence. She had right hemiparesis with bilateral positive Babinski's sign. Additionally, there was bilateral blepharoptosis with right esotropia. With regard to extraocular movement, the patient demonstrated conjugate upgaze palsy and left monocular down gaze palsy (vertical one-and-a-half syndrome: VOHS). Horizontal gaze in the left eye was completely impaired and there was limited abduction of the right eye. Magnetic resonance imaging of the brain showed left thalamo-mesencephalic infarction. On day 4, the vertical eye movement developed into conjugate upgaze and down- gaze palsies. Magnetic resonance imaging of the brain indicated high signal lesion extending into the dorsal portion of the midbrain. It was suggested that the pathway to contralateral downgaze neurons could have been damaged due to the unilateral (left) dosal midbrain lesion before its decussation with the unilateral interstitial nucleus of Cajal, the oculomotor nucleus and the rostral interstitial nucleus of the medial longitudinal fasciculus. This case is considered to be important because there has been no previous report of bilateral vertical gaze palsy due to VOHS in the same patient. Since there are various patterns of ocular movement disorder in the thalamo-mesencephalic portion, careful observations are required to localize the lesions.
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PMID:[Case of unilateral thalamo-mesencephalic infarction with enlargement to bilateral vertical gaze palsy due to vertical one-and-a-half syndrome]. 1823 38

This is a case report of a 15-year-old boy who developed benign intracranial hypertension after 3 weeks of levofloxacin intake. The headache, diplopia, and papilledema resolved within a week after levofloxacin was withdrawn. Physicians must be aware that quinolone antibiotics can potentially cause intracranial hypertension.
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PMID:Intracranial hypertension and levofloxacin: a case report. 1864 80

Antiphospholipid syndrome (APS) is an acquired thrombotic disorder. It mainly occurs with systemic disease or as a primary disorder. All organs may be involved by thrombosis, but to date the most common endocrine manifestation is chronic adrenal insufficiency. Very few cases of hypopituitarism with primary APS have been reported. We report the case of a 27-year-old woman, victim of a stroke leading to double vision and intracranial hypertension. Magnetic resonance imaging showed a macro-adenoma with hemorrhage of a suprasellar lesion. Hormone assessment showed hyper prolactinemia with positive anticardiolipin antibody. Our case is the second reported associating APS with apoplexy. We discuss the clinical, biological and radiological features observed in our case. We conclude that APS should be searched for whenever a history of adenoma with apoplexy is found associated with recurrent thrombosis.
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PMID:[Pituitary necrosis and antiphospholipid syndrome]. 1893 32

We report a case of ruptured tectal arteriovenous malformation (AVM) that was demonstrated angiographically only after removal of an unruptured occipital AVM. A 57-year-old man presented with sudden onset of diplopia and tinnitus. Computed tomography revealed a small hemorrhage in the right tectum mesencephali with intraventricular hemorrhage. Magnetic resonance imaging and angiography disclosed AVM in the right occipital lobe which was separate from the hemorrhagic lesion. Angiography demonstrated that the right occipital AVM was fed by the parieto-occipital artery and drained into the superior sagittal sinus and vein of Galen. However, no abnormal vascular lesion was detected near the tectum mesencephali. As venous hypertension was considered the reason for hemorrhage, the occipital AVM was completely resected. Postoperative angiography demonstrated disappearance of the occipital AVM, but it also disclosed a small tectal AVM fed by branches from the superior cerebellar artery, which had not been detected on preoperative angiography. This was considered the true cause of hemorrhage, and gamma knife surgery was accordingly performed. Even if an AVM is demonstrated, if the lesion does not correspond to the hemorrhage we recommend serial angiographical evaluation so that a small AVM is not missed.
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PMID:Ruptured tectal arteriovenous malformation demonstrated angiographically after removal of an unruptured occipital lobe arteriovenous malformation. 1916

We report a 54-year-old man with right abducent nerve palsy, right facial nerve palsy, and left segmental sensory disturbance, which progressed for 2 weeks. He was found to have cavernous angioma in the lower pons. When he visited our hospital, he had right facial palsy, sensory disturbance of left half of the face and left upper limb, and diplopia. He had suffered right abducent nerve palsy 5 years previously and had recently developed hypertension. Neurological examination further revealed right abducent nerve palsy, right peripheral facial nerve palsy, sensory impairment of the left half of the face, and sensory impairment on the left side from C2 to Th3. Magnetic resonance imaging of the head revealed hemorrhage with a rim at the right dorsal part of the lower pons. No abnormalities were identified on cerebral angiography. He was diagnosed as having hemorrhage originating from a cavernous angioma. We assumed that the segmental sensory disturbance was caused by medial involvement of the lateral spinothalamic tract, which is somatotopically arranged: the fibers from the sacral segments being most lateral. The ventral trigeminothalamic tract, right abducent nerve, and right facial nerve were also disturbed. Segmental sensory disturbance usually accompanies a spinal cord lesion. But several cases with similar symptoms following a brainstem lesion have been reported. Most of them had stroke, showing acute onset of illness. Our case showed subacute onset of illness; cranial nerve palsy and segmental sensory disturbance progressed for 2 weeks.
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PMID:[A case of cavernous angioma in the lower pons, showing subacute onset of unilateral cranial nerve palsy and segmental sensory disturbance]. 1922 94

Although giant cell arteritis (GCA) is a rare cause of ophthalmoplegia, swift diagnosis and treatment are necessary to avoid other complications. We report here a case of GCA in a 59-year-old woman with a history of hypertension and thyroid lobectomy. Diagnosis resulted from binocular diplopia, although classical GCA symptoms had been present a few days before. Oral corticotherapy led to a rapid disappearance of headaches and normal ocular motility in 1 month. We discuss the ophthalmological signs of the disease and the place of temporal artery biopsy and treatment.
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PMID:[Acute diplopia after the age of 50; always look for giant cell arteritis]. 1953 71

Neuropathic arthropathy (Charcot's arthropathy) is a progressive articular disease associated with a reduced sensorial and protector proprioceptive reflex. Its etiology includes many different conditions such as syringomyelia, traumatic lesion causing medullary deformity, spina bifida, diabetic neuropathy, leprosy neuropathy, neurofibromatosis, amyloid neuropathy, alcohol, and repetitive injection of hydrocortisone into joints, among others. However, the relationship between Charcot's arthropathy and herpetic encephalitis has not yet been described. Herpes encephalitis causes acute and chronic diseases of the peripheral or central nervous system. It can manifest as subacute encephalitis, recurrent meningitis, or myelitis. It can also resemble psychiatric syndromes, diplopia, sensory changes in the face and limbs, personality changes, frontal dysexecutive syndrome, stiff neck, subclinical alterations of the vestibular function, intracranial hypertension, convulsion, hemiparesis, and generally includes motor components, among others. On the other hand, pure peripheral sensory disturbance has not been described. In this article, we report the clinical case of a patient with Charcot's arthropathy secondary to pure peripheral sensory polyneuropathy as a consequence of progressive herpetic encephalitis sequelae. In this article, the authors report the first case of Charcot's arthropathy secondary to herpetic encephalitis.
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PMID:Charcot's arthropathy secondary to herpetic encephalitis sequelae: an unusual presentation. 1953 44

We report a patient with carotid cavernous fistula (CCF) presenting with cervical myelopathy. The patient initially presented with ocular pain accompanied by binocular diplopia and was diagnosed with Tolosa-Hunt syndrome at another institution. This patient experienced long-standing venous hypertension due to the delay in diagnosis. Posterior venous drainage from the CCF caused venous congestion in the brainstem and cervical spinal cord causing cervical myelopathy. Glue embolization using n-butyl-2-cyanoacrylate was attempted, but only partial embolization was possible because access to feeding arteries was limited. Stereotactic gamma-knife radiosurgery was performed as an alternative treatment, and effectively obliterated the CCF. However, the patient remained disabled due to cervical cord atrophy associated with long-standing venous hypertension.
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PMID:Carotid cavernous fistula with cervical myelopathy. 1957 Jun 82

We present a patient with a Rathke's cleft cyst who presented with rapidly progressive bilateral 6th nerve palsy. A 20-year-old woman with a history of cleft palate, hypertension, and hydronephrotic kidneys presented with a one month history of headache, associated with dizziness and diplopia on horizontal gaze. Examination was significant for profound bilateral 6th nerve palsies. Magnetic resonance imaging showed a hypodense mass that filled the sella and compressed the right cavernous sinus without contacting the optic chiasm. Pituitary function was normal. An endoscopic, transnasal transsphenoidal resection of the lesion was performed; microscopic examination revealed a Rathke's cleft cyst. Surgical excision resulted in near complete resolution of the bilateral 6th nerve palsy. Rathke's cleft cysts are an unusual cause of bilateral sixth nerve palsy and represent a potential cause of cranial neuropathy.
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PMID:Rathke's cleft cyst presenting as bilateral abducens nerve palsy. 1962 Dec 62


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