Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is an acquired immune-mediated demyelinating neuropathy. In this report, we detail the course of a 58-year-old male patient who had headache and double vision followed by progressive paresthesia and difficulty in walking. The patient had bilateral papilledema and mild leg weakness, absent ankle jerks and loss of sensation in distal parts of his lower and upper extremities. His electromyography (EMG) was concordant with CIDP and lumbar puncture revealed high opening pressure. The polyradiculoneuropathy as well as the papilledema and elevated cerebrospinal fluid (CSF) pressure improved under steroids. The improvement in intracranial hypertension (IHT) and papilledema under steroid treatment suggests that the IHT in this patient might be associated with CIDP.
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PMID:Chronic inflammatory demyelinating polyradiculoneuropathy associated intracranial hypertension. 2294 56

This is an observational case series of five cases of acute acquired comitant esotropia (AACE) with diplopia, aged between 5 and 12 years. The duration of presenting complaints ranged from 4 days to 2 months. A detailed ophthalmic evaluation and neuroimaging were done on all patients. Three patients were found to have intracranial pathology. Two patients had pontine glioma and one patient had benign intracranial hypertension. One patient was diagnosed as accommodative spasm and one patient was diagnosed as having Type 2 AACE.We would like to conclude that AACE can be of a varied aetiology ranging from convergence spasm to those harboring serious intracranial diseases. We reiterate that AACE has a small but significant association with intracranial disorders. Neuroimaging is a definite need in cases which cannot be proved to be either Type 1 or 2.
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PMID:Varied aetiology of acute acquired comitant esotropia: A case series. 2299 65

Two cases of cerebellar tonsilar herniation due to shunt complications in idiopathic intracranial hypertension are reported in which both patients presented with visual symptoms. One patient had horizontal diplopia due to an acute sixth nerve palsy along with severe constriction of visual fields while the second patient had symptoms of blurred vision. Both patients required neurosurgery, one patient requiring surgery for tonsillar descent and revision of an over-draining lumbar peritoneal shunt and the second patient only requiring revision of his over-draining lumbar peritoneal shunt. Following surgery the visual signs of reduced vision, cranial nerve palsy, and visual field loss gradually resolved. Both patients had normal ocular movements and visual fields at final follow-up.
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PMID:Diplopia and visual impairment as presenting symptoms of shunt failure in association with tonsillar herniation in idiopathic intracranial hypertension. 2321 Nov 44

We report on two prepubescent girls with visual loss due to idiopathic intracranial hypertension (IIH), or pseudotumor cerebri, both treated with recombinant human growth hormone for growth failure. The interval from starting hormone therapy to diagnosis of IIH was 3 and 18 months, respectively. Both girls did not complain of headache and nausea. They were neither obese nor did they suffer from renal insufficiency. In both patients, we observed bilateral optic disc edema with visual loss and elevated cerebrospinal fluid (CSF) pressures. Other causes of IIH were excluded with neuroimaging and CSF examination. Cessation of drug administration is often sufficient for symptom resolution in cases of hormone therapy-associated IIH. However, visual field defects in one girl remained unchanged during follow-up of 8 months. In children with IIH, the spectrum of neurologic and visual manifestations might be variable and unspecific. Diagnosis and management of IIH can be difficult in the absence of headache. Blurred or double vision due to cranial nerve palsy might be the only symptom rather than complaints about reduced visual acuity. Therefore, regular clinical monitoring of visual function and fundus appearance is essential for early diagnosis, efficient management, and improvement of visual outcome in children receiving recombinant human growth hormone.
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PMID:Visual loss without headache in children with pseudotumor cerebri and growth hormone treatment. 2327 58

Idiopathic intracranial hypertension (IIH) is defined as a syndrome of increased intracranial pressure without causative lesions on magnetic resonance imaging. The symptoms of IIH patients are headache, transient visual obscurations, photopsia, retrobulbar pain, diplopia, visual loss and papilledema. Management of intracranial hypertension is initially medical, using a combination of managed weight body reduction and diuretic, non-steroid and steroid therapy. Surgical therapy may be required to stabilize vision.
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PMID:[Idiopathic intracranial hypertension and organ of vision]. 2334 7

Idiopathic intracranial hypertension is often believed to be an illness exclusively occurring in obese women in their twenties and thirties. This case describes a four-year-old boy presenting with headache, vomiting photophobia and double vision for six days. He did not have a fever; and all exams and tests, including a magnetic resonance imaging of the brain showed normal values. During the eye examination, he was found to have bilateral papilloedema and when undergoing lumbar puncture an elevated pressure of 230 mm H(2)O was discovered. The patient was diagnosed with idiopathic intracranial hypertension and treated with azetazolamide. Within few days, his symptoms disappeared.
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PMID:[Idiopathic intracranial hypertension is a rare cause of headache in children]. 2346 40

Preeclampsia can cause myriad organ dysfunction, including cranial nerve palsies that pose diagnostic and management dilemmas. We present an unusual case of third nerve palsy, (presenting as diplopia, ptosis) with hypertension, hyperreflexia, proteinuria, easy bruising in a parturient at 34 + 6/52 weeks of twins gestation. She was treated as for severe preeclampsia and HELLP syndrome; intravenous magnesium sulphate and labetalol commenced and emergent cesarean delivery performed under general anesthesia due to concerns of low platelets and for airway protection should her glascow coma scale (GCS) deteriorate. Postoperatively, stroke, aneurysm and intra-cerebral causes of third nerve palsy were excluded, with subsequent recovery of symptoms upon blood pressure normalization. The eye signs are postulated to be due to two preeclamptic mechanisms involving disordered cerebral autoregulation: (1) hyperperfusion and breakdown of the blood-brain barrier that occurs with rising hypertension, causing fluid/blood product extravasation into brain parenchyma, or (2) focal reactive vasoconstriction and local hypoperfusion, contributed to by endothelial dysfunction.
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PMID:Third nerve palsy associated with preeclampsia and HELLP syndrome. 2347 50

A 42-year-old young lady presented with acute onset of dizziness, drooping of left eye with binocular diplopia and inability to walk unassisted. She had past history of uncontrolled diabetes mellitus and hypertension. On examination, she had left fascicular type of third nerve palsy, vertical one and half syndrome (VOHS), left internuclear ophthalmoplegia and skew deviation with ipsilesional hypertropia. She also had thalamic astasia and right unilateral asterixis. Her MRI revealed T2 and Flair hyper intense signal changes with restricted diffusion in the left thalamus, subthalamus and left midbrain. MR Angiography was normal. Thalamic-subthalamic paramedian territory infarct is relatively uncommon. It can present with oculomotor abnormalities including vertical one and half syndrome, skew deviation, thalamic astasia and asterixis. This case is reported for the rarity of the presenting clinical findings in unilateral thalamo-mesencephalic infarcts.
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PMID:Unilateral asterixis, thalamic astasia and vertical one and half syndrome in a unilateral posterior thalamo-subthalamic paramedian infarct: An interesting case report. 2391 12

Mitochondrial disorder (MtD) is usually a multisystem disease due to impaired mitochondrial energy production. Severe hypokalemia resulting in muscle weakness and rhabdomyolysis has not been reported as a phenotypic feature of MtD. Here we describe a 60-year-old male patient who developed myalgias followed by generalized muscle weakness a few days before admission. Symptoms were attributed to severe hypokalemia that occurred after the patient had discontinued spironolactone, a competitive antagonist of the aldosterone receptor, four months earlier on his own judgment. Spironolactone was given for 10 years to treat suspected primary hyperaldosteronism (Conn's syndrome). He presented with myopathic face, bilateral ptosis, hypertelorism, brachydactylia, weakness of the axial and limb muscles, and bilateral leg edema. Hypertelorism and brachydactylia are known as physical traits of MtD. Laboratory investigations revealed hypokalemia of 1.7 mmol/l and elevated serum levels of creatine kinase (2,772 U/l). Electrocardiogram showed sinus rhythm, left bundle-branch-block, repolarization abnormalities, and prolonged QTc (571 ms), which is associated with a propensity to ventricular arrhythmias. Diagnostic work-up revealed bilateral adenomas of the suprarenal glands. Conn's syndrome was regarded as a manifestation of MtD, since MtDs are frequently associated with endocrine abnormalities. The patient also presented with occasional double vision, ptosis, renal insufficiency, bilateral renal cysts, hypertriglyceridemia, arterial hypertension, and hypertrophic cardiomyopathy. Taken together, we have made the diagnosis of MtD. In conclusion, MtD may be associated with adrenal adenomas, which may cause severe symptomatic hypokalemia, manifesting as generalized weakness and myalgias due to rhabdomyolysis. Endocrine involvement may be a phenotypic feature of MtD.
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PMID:Severe hypokalemic paralysis as a manifestation of a mitochondrial disorder. 2398 82

Ischemic abducens nerve palsy usually presents as isolated cranial nerve palsy in the middle aged and elderly patients with known risk factors such as diabetes mellitus, hypertension, dyslipidemia, carotid artery disease, etc., In this report, we describe four patients with isolated abducens nerve palsy who presented with an acute onset diplopia whose detailed history and examination were suggestive of an ischemic etiology. Detailed systemic and laboratory evaluation revealed hyperhomocysteinemia as the only potential risk factor. To the best of our knowledge this is the first report of association of hyperhomocysteinemia and isolated abducens nerve palsy.
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PMID:Isolated abducens nerve palsy with hyperhomocysteinemia: association and outcomes. 2421 15


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