Ear drops for the removal of ear wax

Burton, MJ; Doree, CJ

doi:10.1002/14651858.cd004326

Cited by 54 publications

(48 citation statements)

References 22 publications

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“…Additionally, serum B12 should be checked in all patients with (1) history of gastric bypass surgery, partial or total gastrectomy, terminal ileum disease or resection, or pancreatic insufficiency,14,20,33,200 (2) chronic use of levodopa, histamine type-2 (H2) receptor blockers, or protein pump inhibitors (PPIs),22,33,51,54,342–345 or (3) findings suggestive of (a) behavioral and psychological symptoms of dementia (BPSD), (b) SCD, including paresthesias, ataxia, or loss of position or vibratory senses, or (c) pernicious anemia (PA), including low hemoglobin (Hgb), elevated mean corpuscular volume (MCV), or corpuscular changes on peripheral smear 62. If such findings are absent, and patients have moderately severe to severe dementia of longer than two years duration, then universal recommendations1–4 of assessing for and, when found, treating B12 deficiency may not be supported by reliable evidence 13,16,24,26,92,187,326,346–364. H2 receptor blockers and PPIs impair cobalamin absorption; 18,22,33,365,366 their use is associated with supplemental B12 initiation 367.…”

Section: Discussionmentioning

confidence: 99%

Cobalamin deficiency, hyperhomocysteinemia, and dementia

Werder¹

2010

NDT

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IntroductionAlthough consensus guidelines recommend checking serum B12 in patients with dementia, clinicians are often faced with various questions: (1) Which patients should be tested? (2) What test should be ordered? (3) How are inferences made from such testing? (4) In addition to serum B12, should other tests be ordered? (5) Is B12 deficiency compatible with dementia of the Alzheimer’s type? (6) What is to be expected from treatment? (7) How is B12 deficiency treated?MethodsOn January 31st, 2009, a Medline search was performed revealing 1,627 citations related to cobalamin deficiency, hyperhomocysteinemia, and dementia. After limiting the search terms, all abstracts and/or articles and other references were categorized into six major groups (general, biochemistry, manifestations, associations and risks, evaluation, and treatment) and then reviewed in answering the above questions.ResultsThe six major groups above are described in detail. Seventy-five key studies, series, and clinical trials were identified. Evidence-based suggestions for patient management were developed.DiscussionEvidence is convincing that hyperhomocysteinemia, with or without hypovitaminosis B12, is a risk factor for dementia. In the absence of hyperhomocysteinemia, evidence is less convincing that hypovitaminosis B12 is a risk factor for dementia. B12 deficiency manifestations are variable and include abnormal psychiatric, neurological, gastrointestinal, and hematological findings. Radiological images of individuals with hyperhomocysteinemia frequently demonstrate leukoaraiosis. Assessing serum B12 and treatment of B12 deficiency is crucial for those cases in which pernicious anemia is suspected and may be useful for mild cognitive impairment and mild to moderate dementia. The serum B12 level is the standard initial test: 200 picograms per milliliter or less is low, and 201 to 350 picograms per milliliter is borderline low. Other tests may be indicated, including plasma homocysteine, serum methylmalonic acid, antiparietal cell and anti-intrinsic factor antibodies, and serum gastrin level. In B12 deficiency dementia with versus without pernicious anemia, there appear to be different manifestations, need for further workup, and responses to treatment. Dementia of the Alzheimer’s type is a compatible diagnosis when B12 deficiency is found, unless it is caused by pernicious anemia. Patients with pernicious anemia generally respond favorably to supplemental B12 treatment, especially if pernicious anemia is diagnosed early in the course of the disease. Some patients without pernicious anemia, but with B12 deficiency and either mild cognitive impairment or mild to moderate dementia, might show some degree of cognitive improvement with supplemental B12 treatment. Evidence that supplemental B12 treatment is beneficial for patients without pernicious anemia, but with B12 deficiency and moderately-severe to severe dementia is scarce. Oral cyanocobalamin is generally favored over intramuscular cyanocobalamin.

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Section: Discussionmentioning

confidence: 99%

Cobalamin deficiency, hyperhomocysteinemia, and dementia

Werder¹

2010

NDT

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“…[48] found that vitamin B12 treatment improves cognitive impairment, but does not reverse dementia. Although evidence of vitamin B12 efficacy in improving the cognitive function of people with dementia and B12 serum concentrations is insufficient [49], it is advisable to screen for vitamin B12 in all patients with cognitive impairment [23]. Recently, folic acid and vitamin B supplementation (B12, B6) has been found to slow the atrophy of brain regions that are associated with cognitive decline [50].…”

Section: The Multifaceted Clinical Presentation Of Cobalamin Deficmentioning

confidence: 99%

Cobalamin Deficiency: Clinical Picture and Radiological Findings

et al. 2013

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Vitamin B12 deficiency causes a wide range of hematological, gastrointestinal, psychiatric and neurological disorders. Hematological presentation of cobalamin deficiency ranges from the incidental increase of mean corpuscular volume and neutrophil hypersegmentation to symptoms due to severe anemia, such as angor, dyspnea on exertion, fatigue or symptoms related to congestive heart failure, such as ankle edema, orthopnea and nocturia. Neuropsychiatric symptoms may precede hematologic signs and are represented by myelopathy, neuropathy, dementia and, less often, optic nerve atrophy. The spinal cord manifestation, subacute combined degeneration (SCD), is characterized by symmetric dysesthesia, disturbance of position sense and spastic paraparesis or tetraparesis. The most consistent MRI finding is a symmetrical abnormally increased T2 signal intensity confined to posterior or posterior and lateral columns in the cervical and thoracic spinal cord. Isolated peripheral neuropathy is less frequent, but likely overlooked. Vitamin B12 deficiency has been correlated negatively with cognitive functioning in healthy elderly subjects. Symptoms include slow mentation, memory impairment, attention deficits and dementia. Optic neuropathy occurs occasionally in adult patient. It is characterized by symmetric, painless and progressive visual loss. Parenteral replacement therapy should be started soon after the vitamin deficiency has been established.

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“…Among healthy, older adults, there was no consistent evidence that folic acid supplementation with or without vitamin B12 improved cognitive function. A separate Cochrane database review conducted by Malouf and Sastre (41) reported similar findings in an examination of the effects of B12 on cognition, specifically. Three trials were included, all of which examined this association among individuals with cognitive impairment and low levels of serum B12.…”

Section: Dietary Components and Neurocognitionmentioning

confidence: 54%

Dietary Factors and Cognitive Decline

Smith¹,

Blumenthal²

2015

J Prev Alz Dis

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Cognitive decline is an increasingly important public health problem, with more than 100 million adults worldwide projected to develop dementia by 2050. Accordingly, there has been an increased interest in preventive strategies that diminish this risk. It has been recognized that lifestyle factors including dietary patterns, may be important in the prevention of cognitive decline and dementia in later life. Several dietary components have been examined, including antioxidants, fatty acids, and B vitamins. In addition, whole dietary eating plans, including the Mediterranean diet (MeDi), and the Dietary Approaches to Stop Hypertension (DASH) diet, with and without weight loss, have become areas of increasing interest. Although prospective epidemiological studies have observed that antioxidants, fatty acids, and B vitamins are associated with better cognitive functioning, randomized clinical trials have generally failed to confirm the value of any specific dietary component in improving neurocognition. Several randomized trials have examined the impact of changing ‘whole’ diets on cognitive outcomes. The MeDi and DASH diets offer promising preliminary results, but data are limited and more research in this area is needed.

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Ear drops for the removal of ear wax

Cited by 54 publications

References 22 publications

Cobalamin deficiency, hyperhomocysteinemia, and dementia

Cobalamin deficiency, hyperhomocysteinemia, and dementia

Cobalamin Deficiency: Clinical Picture and Radiological Findings

Dietary Factors and Cognitive Decline

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