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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nine hypertensive children (mean age: 5.0 years (SD: 4.5), range: 10 months to 15 years) were administered nifedipine (capsule) rectally (0.2 to 0.5 mg/kg) when their blood pressures were over 170 mmHg systolic and/or over 110 mmhg diastolic, independent of their ages. The causes of hypertension were acute glomerulonephritis (n = 2), chronic glomerulonephritis (n = 2), renovascular hypertension (n = 4), and polycystic kidney (n = 1). Both systolic and diastolic blood pressures fell in all children after rectal administration of nifedipine, although the response of blood pressure was weak in one child with renovascular hypertension. Blood pressures were lowest at 30 to 60 minutes, and remained under 140 mmHg systolic and 80 mmHg diastolic at least for three hours. Side-effects were headache in one child, palpitations in two children, and facial flushing in three. All of these symptoms were mild, and no special treatment was required. These findings suggest that rectal administration of nifedipine may be effective and the most reliable way to treat young children with severe or urgent hypertension.
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PMID:Rectal administration of perforated nifedipine capsules in acute severe hypertension in children. 145 94

A patient who had bilateral distal anterior cerebral artery aneurysms and a right middle cerebral artery aneurysm in association with polycystic kidney and liver disease is reported. A 57-year-old woman was referred to our center with headache and disturbance of consciousness. On admission, her level of consciousness as evaluated by the Japan Coma Scale was 10. CT revealed subarachnoid hemorrhage, especially in the interhemispheric fissures. Right carotid angiography demonstrated bilateral distal anterior cerebral artery aneurysms and a right middle cerebral artery aneurysm. All three aneurysms were clipped in a one-stage procedure. The patient was discharged without any neurological deficits two weeks after the operation. Bilateral distal anterior cerebral artery aneurysms are extremely rare. This is the first report of such aneurysms and a right middle cerebral artery aneurysm in association with polycystic kidney and liver disease. The etiology of these aneurysms is discussed.
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PMID:[Bilateral distal anterior cerebral artery aneurysms associated with polycystic kidney and liver disease; a case report]. 150 18

Recently, it has been reported that magnetic resonance angiography (MRA) is useful for screening and following up cerebral aneurysms in patients with autosomal dominant polycystic kidney disease (ADPKD). However, a patient was encountered with a ruptured cerebral aneurysm that was not detected by routine MRA. The patient, a 29-year-old man with ADPKD, was followed up at our hospital for more than 5 years. Ten months after an MRA examination, he suddenly developed severe headache. Brain computed tomography revealed subarachnoid hemorrhage. Digital subtraction angiography detected an aneurysm with a diameter of approximately 2 mm in the anterior communicating artery. Clipping of the aneurysm was immediately performed and he recovered without sequela after operation. Magnetic resonance angiography is useful to detect cerebral aneurysms, but it can not detect aneurysms measuring less than 4 mm.
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PMID:Ruptured cerebral aneurysm not detected by magnetic resonance angiography in juvenile autosomal dominant polycystic kidney. 1081 Sep 73

As less arteriography is performed before carotid surgery, concern arises about missing occult cerebral aneurysms and possible adverse outcomes. A study was conducted by the divisions of vascular surgery and neurosurgery of Northwestern University Medical School to evaluate the frequency of incidental cerebral aneurysms and outcomes of patients with extracranial cerebrovascular disease and asymptomatic cerebral aneurysms. From October 1995, through March 1997, 200 patients underwent intracranial and extracranial cerebrovascular angiography for evaluation of extracranial disease. Demographic data, symptoms, data of vascular lesions, surgical treatment and outcomes of stroke and death were recorded prospectively. Two patients (1%) had asymptomatic cerebral aneurysms found on angiography. Six more patients were referred with a known asymptomatic cerebral aneurysm with extracranial disease during this same period. Of these eight patients, five underwent extracranial vascular reconstruction surgery and seven received treatment for their aneurysms. There were two stroke complications, both occurred after treatment of a basilar artery aneurysm. One of these patients died. No aneurysms ruptured following 203 extracranial revascularizations during this same period. On the basis of the low prevalence of diagnosing coincidental cerebral aneurysms during work-up of extracranial disease, as well as the lack of evidence that carotid surgery predisposes to aneurysm rupture in these patients in both our study and the literature review, it is concluded that coexisting extracranial disease and asymptomatic cerebral aneurysms do not pose a case against carotid surgery without routine arteriography. However, arteriography should be considered in selected groups of patients where the yield of intracranial aneurysms is high; these include patients with a familial history of cerebral aneurysms, autosomal dominant polycystic kidney disease, extracranial internal carotid artery medial fibrodysplasia, Takayasu's arteritis, alpha1-antitripsin deficiency and atypical clinical presentations, including headache.
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PMID:Incidental asymptomatic cerebral aneurysms in patients with extracranial cerebrovascular disease: is this a case against carotid endarterectomy without arteriography? 1106 10

It is possible to identify renal cysts in several subjects by ultrasonography imaging techniques. Among the inherited polycystic kidney diseases we include autosomal recessive polycystic kidney disease (ARPKD) and autosomal dominant polycystic diseases such as von Hippel-Lindau disease, tuberous sclerosis complex (TSC1 and TSC2), and autosomal dominant polycystic kidney disease (ADPKD). ARPKD is a rare disease, related to PKHD1 gene, located on chromosome 6p21, that encodes a protein named polyductin/fibrocystin. Pathoanatomical features are bilateral kidney involvement with multiple microcysts, and invariably liver involvement with portal and interlobular fibrosis. A single genetic defect leads to different degrees of renal and hepatic involvement with very different phenotypes and different clinical outcome, in the same family too. ARPKD clinically may show 4 different forms: perinatal, neonatal, infantile, and juvenile. ADPKD is much more frequent (1: 400-1000 live births), and can arise from mutations in 2 different genes, named PKD1 located on chromosome 16p13.3, and PKD2 located on chromosome 4q21-23. The proteins encoded by the PKD1 and PKD2 genes are named polycystins which play crucial roles in several biologic processes. To explain the focal lesions that affected different organs and tissues the "double hit" theory has been proposed (germinal mutation plus somatic mutation on PKD1 or PKD2). Recently, biologic evidence documented the crucial role of the renal primary cilia on the formation of polycystins to induce cystogenesis. ADPKD may be clinically characterized by abdominal pain, hypertension, episodes of gross hematuria, headache, renal stones, aortic and cerebral aneurysms, mitral valve prolapse, and polycystic liver disease. ADPKD is slowly progressive disease responsible for up 10% of end stage renal failure (ESRF) in every country of the world. Male sex, PKD1 gene, episodes of gross hematuria, and the precocity and severity of hypertension play an important role in the progression of renal disease to ESRF.
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PMID:Autosomal recessive and dominant polycystic kidney diseases. 1578 25

We report the case of a 60-year-old woman with autosomal dominant polycystic kidney disease (ADPKD) that presented with headache and right complete ophthalmoplegia. The CT scan raised the possibility of a giant aneurysm of the right intracavernous internal carotid artery, confirmed by angiography. The patient underwent endovascular occlusion of parent vessel with detachable coils, then she presented interruption of headache and partial recovery of ptosis and ophthalmoplegia. We emphasize the relationship between ADPKD and intracranial aneurysms. We also discuss the natural history and compare the therapeutic options for the management of giant aneurysms of the cavernous portion of the carotid artery.
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PMID:[Giant aneurysm of the intracavernous internal carotid artery associated with autosomal dominant polycystic kidney disease: case report]. 1705 4

We report a rare case with polycystic kidney disease (PKD) having an intracranial internal carotid artery aneurysm associated with extracranial occlusion of the ipsilateral internal carotid artery. A 55-year-old man with chronic renal failure due to PKD presented with headache. CT scan and MRI showed no abnormal findings. MRA showed cervical occlusion of the right internal carotid artery and an ipsilateral intracranial carotid aneurysm. At surgery, the saccular aneurysm protruded anterolaterally at the C2 portion of the right internal carotid and was clipped. Hemodynamic stress of the blood flow through the posterior communicating artery and the fragility of arteries because of PKD were considered to be two main causes of aneurysmal formation in this case.
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PMID:[Intracranial internal carotid artery aneurysm associated with extracranial occlusion of the ipsilateral internal carotid artery in a patient with polycystic kidney disease]. 1804 27

Intracranial hypotension is typically manifested by orthostatic headache. The most frequent underlying factor is cerebrospinal fluid leakage. It has been suggested that dural structural weakness in some connective tissue diseases may be responsible for dural tears and diverticula and consequently leakage. We present a case of spontaneous intracranial hypotension associated with Marfan syndrome and autosomal dominant polycystic kidney disease. The patient was treated successfully with epidural autologous blood patch. Dural involvements of these hereditary connective tissue diseases are also discussed.
Headache 2008 Apr
PMID:Spontaneous intracranial hypotension syndrome in a patient with marfan syndrome and autosomal dominant polycystic kidney disease. 1819 97

Thirty cases of autosomal dominant polycystic kidney disease (ADPKD) seen at King Fahd Hospital of the University, Al-Khobar over a period of eight years, were analysed with respect to clinical features, laboratory investigations, radiological findings, complications and outcome. There were 13 males and 17 females with a mean age of 45 yrs + 10.1 (range 16-65 years). There was positive family history of renal disease in 17 cases. At the time of presentation, 27 cases had abdominal pain. The other features noted were hematuria (20 cases), polyuria (10 cases), urinary tract infection (22 cases), headache (9 cases), uremia (7 cases) and nephrolithiasis (5 cases). Bilaterally palpable kidneys were present in all cases. Hypertension (17 cases) was the next common clinical finding. Other clinical features noted were hepatomegaly (5 cases) and mitral valve prolapse (5 cases). Twenty-one patients had cysts in liver and five had cysts in spleen. Varying degrees of renal failure were seen in 15 cases. Six (20%) patients progressed to end stage renal disease during the period of observation.
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PMID:Autosomal dominant polycystic kidney disease: observations from a university hospital in saudi arabia. 1858 40

Spontaneous spinal CSF leaks are best known as a cause of orthostatic headache, but may also be the cause of coma. The authors encountered a unique case of a spontaneous spinal CSF leak causing coma 2 days after craniotomy for clipping of an unruptured aneurysm. This 44-year-old woman with autosomal dominant polycystic kidney disease underwent an uneventful craniotomy for an incidental anterior choroidal artery aneurysm. No intraoperative spinal CSF drainage was used. Two days after surgery the patient became comatose with a left oculomotor nerve palsy. Computed tomography scanning revealed a right extraceberal hematoma and loss of gray-white matter differentiation. The hematoma was evacuated and a diagnosis of hemodialysis disequilibrium syndrome was made. Continuous hemodialysis and hyperosmolar therapy were instituted without any improvement. The CT scans were then reinterpreted as showing sagging of the brain, and the patient was placed in the Trendelenburg position which resulted in prompt improvement in her level of consciousness. A CT myelogram demonstrated an upper thoracic CSF leak that eventually required surgical correction. The patient made a complete neurological recovery. Neurological deterioration after craniotomy may be caused by brain sagging caused by a spontaneous spinal CSF leak, similar to intracranial hypotension due to intraoperative lumbar CSF drainage.
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PMID:Spontaneous spinal cerebrospinal fluid leak as a cause of coma after craniotomy for clipping of an unruptured intracranial aneurysm. 1901 77


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