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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of the study was to study admission delay in patients with stroke, and to analyze the influence of demographic, medical, and pathophysiological factors on admission delay. The study was prospective and consecutive and included 1197 unselected patients admitted with acute stroke from a well-defined catchment area in Copenhagen. Only 35% were admitted within the first six hours from stroke onset, and 50% of the patients were admitted later than 14 hours from stroke onset. Living alone (OR 1.75, 95% CI 1.3 to 2.3) and retired working status (OR 1.6, 95% CI 1.01 to 1.54) delayed admission. A well-functioning social network thus seems important to early admission. The milder the stroke, the higher was the risk of delayed admission (OR 1.25 per 10 points increase in stroke severity (Scandinavian Neurological Stroke Scale on admission), 95% CI 1.06 to 2.54. Other factors such as age, sex, diabetes, hypertension, ischaemic heart disease, other comorbidity, previous stroke, headache, aphasia, apraxia, anosognosia, neglect, lowered consciousness, mental status, and type of stroke had no independent influence on admission time. However, a history of TIA increased the chance of early admission by odds 1.64 (95% CI 1.01 to 2.54), indicating that an increase in public awareness and knowledge may reduce delay and save precious time.
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PMID:[Pattern of admissions of patients with apoplexy. Time connection between symptom onset and admission and relation to medical and social factors. The Copenhagen Stroke Study]. 946 80

We reported a 67-year-old woman with bilateral caudate head infarcts. She developed sudden mutism followed by abulia. She was admitted to our hospital 2 months after ictus for further examination. She showed prominent abulia and was inactive, slow and apathetic. Spontaneous activity and speech, immediate response to queries, spontaneous word recall and attention and persistence to complex programs were disturbed. Apparent motor disturbance, gait disturbance, motor aphasia, apraxia and remote memory disturbance were not identified. She seemed to be depressed but not sad. Brain CT and MRI revealed bilateral caudate head hemorrhagic infarcts including bilateral anterior internal capsules, in which the left lesion was more extensive than right one and involved the part of the left putamen. These infarct locations were thought to be supplied by the area around the medial striate artery including Heubner's arteries and the A1 perforator. Digital subtraction angiography showed asymptomatic right internal carotid artery occlusion. She bad had hypertension, diabetes mellitus and atrial fibrillation and also had a left atrium with a large diameter. The infarcts were thought to be caused by cardioembolic occlusion to the distal portion of the left internal carotid artery. Although some variations of vasculature at the anterior communicating artery might contribute to bilateral medial striate artery infarcts, we could not demonstrate such abnormalities by angiography. Bilateral caudate head infarcts involving the anterior internal capsule may cause prominent abulia. The patient did not improve by drug and rehabilitation therapy and died suddenly a year after discharge.
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PMID:[Bilateral caudate head infarcts]. 950 74

We describe the unusual case of a 63-year-old woman with a history of arterial hypertension who presented a sudden weakness of the lower limbs followed by mutism, akinesia and dyspraxia. Magnetic resonance images showed a bilateral medial frontal infarction. Digital subtraction angiography documented a right azygous anterior cerebral artery with severe stenosis in its sub-callosal tract; the left anterior cerebral artery showed mild hypoplasia with only sub-frontal and fronto-polar branches. No embolic source was documented. Afterwards the patient presented a gradual and partial recovery of both motor and cognitive functions.
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PMID:Bilateral medial frontal infarction in a case of azygous anterior cerebral artery stenosis. 1093 47

The cases of three children, 16, 12, and 12 years of age, who suffered sudden confusional state and cortical blindness lasting 12 to 30 minutes while under treatment with high-dose methotrexate, cyclophosphamide, and dactinomycin for a lower limb osteosarcoma are reported. Transient neuropsychologic deficits arose after the acute phase of treatment: left hemispatial neglect and constructive apraxia (Patient 1); constructive apraxia (Patient 2); and constructive apraxia and alexia without aphasia (Patient 3). The three patients recovered completely from all their deficits within the time frame of 3 hours to 2 weeks. Arterial hypertension and hypomagnesemia were found during the acute phase in all patients. In Patients 2 and 3, magnetic resonance imaging revealed increased parieto-occipital T(2) signal involving gray and white matter. In Patients 1 and 2, HmPAO-SPECT revealed parieto-occipital hypoperfusion that resolved a few days later. The alterations detected by neuroimaging were concurrent with the appearance and disappearance of the clinical symptoms. Such transient acute episodes have been named occipital-parietal encephalopathy. On the basis of our clinical, laboratory, and neuroimaging findings, an explanation for the origin of this syndrome, a migrainelike mechanism, triggered by chemotherapy-induced hypomagnesemia, is proposed.
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PMID:Transient posterior encephalopathy induced by chemotherapy in children. 1127 65

Dementia is the development of multiple cognitive deficits that includes memory impairment and at least one of the following--Aphasia, apraxia, agnosia or disturbances in executive functioning. The common causes of dementia among the elderly are Alzheimer's disease, vascular dementia, mixed dementia and Lewy body disease. The concept of reversible dementia was introduced in 1980 when a task force sponsored by National Institute of Ageing found 10-12% of dementia cases in older group to have reversible causes such as metabolic-nutritional, drugs, infections, psychiatric disorders etc. In our series of 76 patients in the presenile age group (<65 years), 34.21% (26/76) had a reversible condition underlying the dementia. 43.42% (33/76) had vascular dementia, 13.15% (10/76) had Alzheimer's disease and 9.21% (7/76) had mixed dementia. Hypertension, hyperlipidemia and diabetes mellitus were commoner in the vascular dementia group as compared to the Alzheimer's group. Evaluation of MRI as a tool in diagnosis of dementia showed increased sensitivity of MRI towards detecting lacunes. The potentially reversible dementias comprised infections 14.47% (11/76), metabolic-nutritional 14.47% (11/76) and autoimmune diseases 3.94% (3/76). These were characterized by a subcortical dementia. Four month follow up of MMSE in this group showed significant and sustained improvement in the metabolic nutritional group.
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PMID:Presenile dementia--etiology, clinical profile and treatment response at four month follow up. 1588 51

The term cognitive impairment of vascular origin is used to designate global cognitive deficits as well as focal neurological deficits such as aphasia, apraxia and agnosia of vascular/circulatory origin. It has been useful for identifying early clinical and neuroradiological alterations that might permit therapeutic strategies geared to curbing the progression of cerebrovascular disease. Multi-infarct encephalopathy, infarcts in strategic areas, lacunae and lacunar status, Binswanger's encephalopathy, hippocampal sclerosis, cortical granular atrophy and watershed infarcts are common lesions. Hypertension and vascular diseases such as arteriosclerosis, small blood vessel disease, inflammatory diseases of the blood vessels, Sneddon syndrome, cerebral amyloid angiopathies, cerebral autosomic dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), and Maeda's syndrome are causative of cognitive impairment of vascular origin. Other less common causes are hereditary endotheliopathy with retinopathy, neuropathy and strokes (HERNS), cerebro-retinian vasculopathy (CRV), hereditary vascular retinopathy (HVR) (all three linked to 3p21.1-p21.3), hereditary infantile hemiparesis with arteriolar retinopathy and leukoencephalopathy (HIHRATL) (not linked to 3p21), fibromuscular dysplasia, and moya-moya disease. Lack of uniformity of clinical manifestations, the variety of vascular diseases and circulatory factors, the diverse, but often convergent, neuropathological substrates, and the common association with unrelated neurodegenerative diseases in the elderly, make it hard to assume a single clinical approach in the diagnosis and treatment of cognitive impairment of vascular origin. Rather, environmental and genetic risk factors, underlying vascular diseases, associated systemic, metabolic and neurodegenerative diseases and identification of extent and distribution of lesions with morphological and functional neuroimaging methods should be applied in every individual patient.
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PMID:Cognitive impairment of vascular origin: neuropathology of cognitive impairment of vascular origin. 2084 74

Cockayne is a segmental progeroid syndrome that has autosomal recessive inheritance pattern. It is mainly characterized by Intrauterine growth retardation, severe postnatal growth deficiency, cachectic dwarfism, microcephaly, wizened face, sensorineural hearing loss, cataracts, dental caries, cardiac arrhythmias, hypertension, atherosclerosis, proteinuria, micropenis, renal failure, skeletal abnormalities, skin photosensitivity, decreased subcutaneous adipose tissue, cerebral atrophy, dementia, basal ganglia calcifications, ataxia and apraxia. It has a complex phenotype given by genetic heterogeneity. There are five gene responsible for this syndrome: CSA, CSB, XPB, XPD and XPG, in which various mutations have been found. The biochemical effect of these mutations includes dysfunctional protein of the repair system for oxidative damage to DNA, the complex coupled to transcription and the nucleotide excision repair system. Considering the role played for these proteins and its effects on clinical phenotype when they are deficient, we suggest that these genes might be candidates for analyzing susceptibility to common chronic degenerative diseases related to oxidative stress and aging.
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PMID:[The metabolic and molecular bases of Cockayne syndrome]. 2141 36

The authors report a case of atherosclerotic stroke in a 46-year-old recreational bodybuilder with a 20 year history of anabolic-adrenergic steroid (AAS) abuse. Cerebrovascular accident (CVA) occurred during his third week of hospital admission for an acute abdomen and on day 8, postemergency laparotomy. CVA presented with collapse, generalised seizures, reduced Glasgow Coma Score and severe hypertension. He was subsequently admitted to the intensive care unit (ICU), where initial investigations did not illustrate an underlying diagnosis. By day 4 in ICU, there had been no significant clinical improvement and radiological investigations were repeated, identifying a left frontal lobe infarct in the middle cerebral artery territory. The authors propose CVA was secondary to AAS. After a prolonged and complicated period of rehabilitation, he has been discharged home; he requires carers due to dyspraxia and is mobilising independently.
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PMID:Delayed diagnosis of a cerebrovascular accident associated with anabolic steroid use. 2820 81

Neuronopathic Gaucher disease can present as a continuum of clinical findings, including somatic symptoms of anemia, thrombocytopenia, hepatosplenomegaly, and bone disease as well as neurologic sequelae. There is a spectrum of neurologic symptoms ranging from oculomotor apraxia to severe convulsions. The heterozygosity of phenotypes makes it difficult to predict the disease course. We describe an 8-year-old male with neuronopathic type III Gaucher disease who developed bladder dysfunction and was unable to completely void. He also presented with hypertension and acute renal insufficiency, most likely secondary to urinary retention. A complete evaluation was done for causes of urinary retention and bladder dysfunction. A renal bladder ultrasound demonstrated marked hydroureteronephrosis. There was no clinical evidence of infection and cystoscopy revealed no anatomic obstruction. In addition, MRI showed no spinal abnormalities. His bladder dysfunction was managed operatively by creating a catheterizable stoma, using his appendix, to empty his bladder, and surgical findings were consistent with neurogenic bladder. He continues to be managed for his Gaucher disease and neurogenic bladder by genetics, nephrology and urology. This is the first clinical report of neurogenic bladder dysfunction in neuronopathic Gaucher disease.
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PMID:Neurogenic bladder dysfunction presenting as urinary retention in neuronopathic Gaucher disease. 2466 77

A 78-year-old Caucasian man was admitted in the Department of Neurology for visual disturbances, started two days before. The next day the patient experienced headache, fever and gait disturbances. He had hypertension, diabetes mellitus, an ischemic stroke 13 years ago, longstanding seronegative rheumatoid arthritis (17 years), polynodular goiter, right ischio-pubian fracture and right femoral vein thrombosis a year ago due to a car accident, since he is treated with oral anticoagulants associated to antiaggregant, hypotensors, statin and oral antidiabetics. The neurologic examination had evidenced nuchal rigidity, left homonymous hemianopsia, left central facial palsy, ataxia of the inferior limbs with wide-based gait, achilean reflexes abolished bilaterally, bilaterally abolished plantar reflexes, ideomotor apraxia, dysarthria, hypoprosexia, and preserved consciousness patient. A non-contrast cerebral CT scan had shown right temporal and parieto-occipital intraparenchymatous hemorrhages, a right frontal sequelar lesion, multiple old lacunar infarets, cortical atrophy. Laboratory findings included an inflammatory syndrome, absence of rheumatoid arthritis positive serology, normal coagulogram, an elevated proteinuria. The cerebral IRM performed on the seventh day of hospitalisation was suggestive for subacute right parietal hemorrhage, old cerebral infarction in the right anterior cerebral artery area, old lacunar infarcts and cerebral atrophy. The anticoagulant and antiaggregant treatment was stopped after a generalized tonic-clonic seizure occurred. Antiedematous, hypotensor, anticonvulsivant, beta-blocker, and symptomatic treatment was started, while the antidiabetic treatment was continued. All symptoms remitted. Arguments for amyloid angiopathy in our patient are previous non-cardioembolic ischemic stroke and a chronic inflammatory disease- rheumatoid arthritis in his personal medical history.
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PMID:Multiple Intracerebral Hemorrhages in an Old Patient with Rheumatoid Arthritis. 2693 15


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