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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

Infective endocarditis, a serious microbial infection of the cardiac endothelial surface, may involve any heart valve. However, right-sided endocarditis is uncommon in non-intravenous drug abusers without underlying heart disease, and the contextual involvement of the left-sided valve is exceptional. A 63-year-old man with no evidence of intravenous drug abuse or heart disease, presented with persistent fever, worsening of breath, and aphasia. His medical history was notable for mild arterial hypertension and serious lymphangitis with cutaneous erosions on the legs. Transesophageal echocardiography was performed for suspicious endocarditis and showed a pedunculated and highly mobile vegetation adhered to the atrial portion of the posterior leaflet of the mitral valve, protruding into the left ventricle through the valvar orifice. Another large vegetation was seen at the tricuspid valve surface and protruded into the right ventricle during diastole. Cerebral and thoraco-abdominal computed tomography scan revealed multiple embolism to the left kidney, spleen, lungs and central nervous system. Blood cultures identified Staphylococcus aureus. The only risk factor was large skin sepsis. Despite successful antibiotic therapy, the patient died for development of renal and respiratory failure.
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PMID:[Widespread embolism in tricuspid and mitral endocarditis caused by chronic lymphangitis. Case report]. 1653 26

The etiology of cerebral hemorrhage is not always easy to diagnose and modern neuroimaging methods may be deceptive. The authors report on a 48-year-old previously healthy male admitted to hospital with a first-time severe generalized epileptic seizure. The patient presented with aphasia, confusion, headaches, nausea, right hemianopia and early papilledema. CT revealed an intracerebral hematoma in the left occipital lobe but MRI and MRA failed to provide any further insight into the etiology of the hemorrhage. Due to persisting intracranial hypertension, the patient underwent neuroendoscopic removal of the hematoma. After blood clots were evacuated, pathologic vascularity was found. Tissue samples were collected from the walls of the hematoma cavity. Neoplastic cells adjacent to the blood vessels were identified in one of the samples. The patient was reoperated and a glioma-like tumor was removed. The diagnosis of cerebral intratumoral hemorrhage is difficult especially when there are no previous clinical signs of a tumor. Neuroendoscopy may speed up the diagnostic process which usually extends past resorption of the haematoma and the technique may be an alternative to stereotactic surgery.
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PMID:[Endoscopic method in etiological diagnosis of spontaneous intracerebral hemorrhage. Case report]. 1687 45

A 77-year-old man who was suffering from an intracerebral hemorrhage of the left subcortex without hypertension was admitted to our hospital. The only neurological symptom was right arm monoparesis. Brain MRI demonstrated a subarachnoid hemorrhage (SAH) in the left frontal lobe. On the day of admission, conventional cerebral angiography revealed no abnormalities in brain arteries. His symptom was disappeared immediately after admission. He was discharged without neurological deficit on day 25. However, he was rehospitalized in our hospital on the same day because he experienced a right subcortical hemorrhage. The neurological symptoms were consciousness disturbance, aphasia and right hemiparesis. Brain CT disclosed a subcortical hemorrhage in the left temporal lobe. CT stereo-guided drainage was performed. Then, we examined tissue removed from the brain's surface. Histologically, beta-amyloid protein was deposited on the walls of the meningeal and cortical vessels, and it replaced all the layers of those walls. Therefore, a diagnosis of cerebral amyloid angiopathy (CAA) was made. His condition gradually improved, but CT showed an asymptomatic ICH in the right parietal lobe on day 36. On day 47, he had a symptomatic ICH in the left caudate nuclei and right frontal lobe. He died on day 66 because of pneumonia. Intracranial hemorrhages due to CAA have been reported and the majority of the lesions have been lober hemorrhage. To the best of our knowledge, few reports have been published regarding primary SAH caused by CAA. The cause of SAH should be considered as CAA when SAH appears without hypertension or in elderly patients.
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PMID:[A case of primary subarachnoid hemorrhage due to cerebral amyloid angiopathy]. 1749 36

Intracranial dural arteriovenous fistulas (AVFs) are potentially at risk for hemorrhage, and their symptoms and prognosis are highly variable. We present 7 surgical cases with the initial symptoms of venous ischemia by dural AVF. The series comprises 3 male and 4 female, ranging in age from 37 to 76 years (mean age, 61.1 years). Initial symptoms were dizziness in 3 cases, headache in 2 cases, unconsciousness in 1 case, and hemiparesis in 1 case. The locations included the superior sagittal sinus in 3 cases and the transverse-sigmoid sinus in 4 cases. Computed tomography with contrast media and magnetic resonance imaging revealed abnormal vessels. In all cases, retrograde feeding into the cortical veins was observed. On angiography, multiple retrograde venous drainage into the cortical veins were observed in all cases. Single photon emission computed tomography (SPECT) demonstrated apparent hypoperfusion in all 7 cases and further decrease by diamox challenging test in 4 cases. The dural AVFs were removed, and the symptoms disappeared in all cases, although transient aphasia was observed in a single case postoperatively. Postoperative SPECT showed improvement of cerebral blood flow in 4 and no change in 2 of 6 follow-up cases. Cerebral ischemia was induced by venous hypertension, and the hypoperfused brain improved immediately after the operation. Cerebral venous ischemia is a reversible condition that can be improved by appropriate early-stage treatment.
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PMID:Cerebral venous ischemia by dural arteriovenous fistulas. 1790 17

Alzheimer's disease is the most prevalent and common form of cognitive impairment, ie, dementia, in the elderly followed in second place by vascular dementia due to the microangiopathy associated with poorly-controlled hypertension. Besides blood pressure elevation, advancing age is the strongest risk factor for dementia. Deterioration of intellectual function and cognitive skills that leads to the elderly patient becoming more and more dependent in his, her, activities of daily living, ie, bathing, dressing, feeding self, locomotion, and personal hygiene. It has been known and demonstrated for many years that lowering of blood pressure from a previous hypertensive point can result in stroke prevention yet lowering of blood pressure does not prevent the microangiopathy that leads to white matter demyelinization which when combined with the clinical cognitive deterioration is compatible with a diagnosis of vascular dementia. It is known from many large studies, ie, SHEP, SCOPE, and HOPE, that lowering of blood pressure gradually will not and should not worsen the cognitive impairment. However, if the pressure is uncontrolled a stroke which might consequently occur would further worsen their cognitive derangement. So an attempt at slow reduction of blood pressure since cerebral autoregulation is slower as age increases is in the patient's best interest. It is also important to stress that control of blood glucose can also be seen as an attempt to prevent vascular dementia from uncontrolled hyperglycemia. Vascular dementia is not considered one of the reversible causes of dementia. Reversible causes of cognitive impairment are over medication with centrally acting drugs such as sedatives, hypnotics, antidepressants, and antipsychotics, electrolyte imbalance such as hyponatremia, azotemia, chronic liver disease, and poor controlled chronic congestive heart failure. Criteria for the clinical diagnosis of vascular dementia include cognitive decline in regards to preceding functionally higher level characterized by alterations in memory and in two or more superior cortical functions that include orientation, attention, verbal linguistic capacities, visual spacial skills, calculation, executive functioning, motor control, abstraction and judgment. Patients with disturbances of consciousness, delirium (acute confusional states), psychosis, serious aphasia, or sensory-motor alterations that preclude proper execution of neuro-psychological testing are also considered to have probably vascular dementia. Furthermore, these are ten of the other essential cerebral or systematic pathologies present that would be able to produce a dementia syndrome.
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PMID:Hypertension and cognitive function in the elderly. 1809 Aug 79

A 75-year-old right-handed woman was admitted to our hospital because of sudden onset of consciousness disturbance. She had taken angiotensin converting enzyme (ACE) inhibitor for hypertension. A neurological examination showed consciousness disturbance, total aphasia, right central facial palsy and right hemiparesis. Diffusion-weighted imaging revealed hyper-intense lesions in the middle cerebral artery territory, particularly in the insular cortex. Magnetic resonance angiography demonstrated occlusion of the left middle cerebral artery. Electrocardiogram monitoring during hospitalization detected an atrial fibrillation. Therefore, we diagnosed her as cardioembolic stroke. She was treated with intravenous alteplase of 0.6 mg/kg. Sixty minutes after alteplase infusion, she developed orolingual angioedema. Immediately she was treated with methylprednisolone intravenously, and the angioedema improved. Orolingual angioedema should be considered as a complication associated with alteplase in a patient who has taking ACE inhibitor.
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PMID:[Orolingual angioedema as complication after rt-PA in stroke patient treated with ACE inhibitor]. 1845 63

We report a case of calcified aortic stenosis revealed by an ischemic stroke. An 81-year-old man with hyperlipidemia, hypertension and renal function impairment presented with acute onset of right-sided hemiparesis and aphasia. Head CT scan revealed a rounded calcified high-density mass within the distal segment of the left anterior cerebral artery, consistent with a calcified cerebral embolus, and an infarct in the left paracentral lobule. Transesophageal echocardiography demonstrated a sclerotic aortic valve. The patient was discharged from hospital on aspirin and atorvastatin, and the outcome was favorable. Calcified embolus remains a rare event and it has been not yet reported in the territory of anterior cerebral artery. It may be observed in aortic and mitral valve diseases, calcified plaques of the internal carotid artery and aortic arch. Renal failure promotes their development and is the cause of cardiovascular diseases. To date, aortic valve calcification is not considered as a marker of stroke risk, except when associated with severe stenosis or left ventricular hypertrophy.
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PMID:[Stroke due to spontaneous calcified cerebral embolus as presenting feature of calcified aortic stenosis]. 1845 37

The study was a cross sectional study conducted among 48 stroke patients in Medicine & Neuromedicine department of Mymensingh Medical College & Hospital. The objective of the study was to reveal the risk factors and other relevant information & immediate outcome of stroke patients. The sample size was 48 who were selected purposively and study area was selected for easy access. Study period was from 15th May 2007 to 15th July 2007. Forty eight (48) respondents and their reliable attendants were interviewed by pre tested structured questionnaire. Among 48 stroke patients 60% were male& 40% were female. Occupations of the patients were 21% desk job, 15% laborious work, 37% housewife, 6% businessman &21% in other profession. Age group of respondents were 13% below 45 years of age, 25% were 45-55 years of age, 29% were 55-65 years of age & 33% were over 65 years of age. Among 48 stroke patients 62.5% had 1st attack & others had multiple attacks. Among all the stroke patients 37.5% performed physical exercise. Forty six percent (46%) patients have family history of Hypertension. 27% have no family history of Hypertension & 27% have no idea. Sixty six percent (66%) patients have suffering from Hypertension, 23% have no history of Hypertension & 10% have no idea. Sixty percent (60%) patients had habit of Smoking, 40% had no habit of Smoking. 21% patients have family history of Diabetes, 48% have no family history of Diabetes & 31% have no idea about family history of Diabetes. Complications among stroke patients are 51% have Hemiplegia, 10% have Paraplegia, 23% have Paresis, 10% have Aphasia & 6% have others complications.
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PMID:Epidemiological study of risk factors of stroke and its immediate consequence. 1862 44

We report on a 78-year-old woman patient with macrothrombocytopenia with leukocyte inclusions (MTCP, May-Hegglin anomaly/Sebastian syndrome), who had no history of hemorrhagic symptoms and had a platelet count of 10,000 or less, but had a cerebral infarction. The patient was found to have idiopathic thrombocytopenic purpura, hypertension, and atrial fibrillation 16 years ago, yet received no medication. She was found to have had a cerebral infarction with aphasia as the chief complaint and was admitted to our hospital. Thrombocytopenia was found in three family members. Blood examinations revealed normal bleeding time and platelet aggregation ability. The patient was found to have the triad of giant platelets, thrombocytopenia, and inclusion bodies in leukocytes. Genetic analysis showed a mutation of the MYH-9 gene in the patients second daughter. Consequently, this patient received a diagnosis of MTCP. There have only been a few reports of the onset of thrombosis in patients with MTCP and no reports of the onset of cerebral infarction. Our report is the first case of MTCP in a patient with cerebral infarction.
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PMID:Cerebral infarction in a patient with macrothrombocytopenia with leukocyte inclusions (MTCP, May-Hegglin anomaly/Sebastian syndrome). 1878 Oct 47


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