Differential diagnosis of Alzheimer's disease

The differential diagnosis of Alzheimer's disease has dramatically changed since the evolution of the diagnostic strategies (with definition of neuropsychological, behavioural, and imaging patterns) and disposal of cholinergic drugs indicated in Alzheimer's disease. The question is no more centred on exclusion of the traditional reversible dementias or depression. It is centred on the distinction between Alzheimer's disease and other degenerative diseases still often misdiagnosed with Alzheimer's disease such as frontotemporal dementias, dementia with Lewy bodies, and some focal atrophies that do not have the same physiopathology and should not be treated with anticholinesterase drugs. Besides, better knowledge on the links between cerebrovascular pathology and Alzheimer's disease, remind us that both pathologies may coexist and should be taken into account.     

Paget's disease and sensori-neural deafness: temporal bone histopathology of Paget's disease

Four cases with Paget's disease of the temporal bone are presented to illustrate the pathogenesis of the associated deafness. One case illustrates the combination of severe deafness due to bilateral otosclerosis with probably asymptomatic bilateral Paget's disease. One case with advanced Paget's disease presents features to explain early stages of sensori-neural deafness before actual cellular invasion of the inner ear. One case of profound deafness due to Paget's disease presents a different stage of cellular invasion of the inner ear by the disease on each side. One case illustrates invasion of the internal auditory meatus by Paget's disease with infiltration of the acoustic division of the nerve and profound deafness.     

The pathogenesis, diagnosis and control of Johne's disease

Since 1962, when the control of Johne's disease was last reviewed by the BVA technical development committee there have been no dramatic advances in diagnostic methods for Johne's disease or in methods of control. However, there has been a slow, but steady increase in knowledge of the various aspects of the disease. This article attempts to set out what is known and, more important, not known about the subject.     

Paget's disease of bone

Paget's disease of bone is a localized disorder of bone remodeling. Increased numbers of larger than normal osteoclasts initiate the process at affected skeletal sites, and the increase in bone resorption is followed by an increase in new bone formation, altering bone architecture. The signs and symptoms of Paget's disease are varied, depending in part on the location of the involved sites and the degree of increased bone turnover. Recent progress in Paget's disease research includes new data regarding the etiology of this disorder and the ongoing development of more effective therapies. Although the cause of Paget's disease remains unproven, the creation of pagetic osteoclasts seems ever more likely to result from both genetic and environmental factors. Many studies indicate that in patients with Paget's disease, both osteoclasts and their precursors harbor evidence of a paramyxovirus infection, although not all studies confirm this finding. Very recent genetic investigations have identified one candidate gene on chromosome 18q, although genetic heterogeneity is almost certainly present. Advances in treatment have resulted from the availability of several potent bisphosphonate compounds (e.g., pamidronate, alendronate, and risedronate) that, unlike earlier treatments, produce normal or near normal bone turnover indices in a majority of patients. New bone formation after such treatment has a more normal, lamellar pattern, and mineralization abnormalities are rare to absent with the newer compounds. The availability of such agents has prompted a more aggressive management philosophy in which both symptomatic disease and also asymptomatic disease at sites with a risk of progression and future complications are viewed as clear indications for pharmacologic intervention.     

Diphosphonate treatment of Paget's disease

Ethane-1-hydroxy-1, 1-diphosphonate (EHDP) was administered in a dose of 20 mg/kg/d to 21 patients with symptomatic Paget's disease. All patients were treated for 6 months and then followed for an additional 6 months. There was a striking decline in serum alkaline phosphatase and urinary hydroxy-proline excretion observed after 3 months of therapy which was not significantly improved in the succeeding 3 months. Concomitantly there was marked improvement in clinical symptoms and bone scans. Following cessation of therapy, continued biochemical and clinical evidence of remission persisted. Several patients on repeat treatment with EHDP appeared to respond promptly. Side effects were minimal except for a possibly related osteomalacia and increased incidence of pathologic fractures.     

Spells. Differential diagnosis and management strategies

In summary, when approaching the patient who has had a spell of unknown cause, the most important differentiation to make is between a syncopal episode and a seizure. The history and physical examination will provide the diagnosis in approximately 85% of cases. Once the physician has some idea of which path to pursue, it is important to order the tests in a directed fashion tailored to the patient's presentation. A shotgun approach is neither warranted nor beneficial and is best avoided when possible. Some patients will remain without a diagnosis despite a complete workup, thus it is important for the emergency physician to rule out the life-threatening possibilities and to arrange the appropriate long-term follow-up for the patient with their primary care provider.     

Actinic keratoses. Differential diagnosis and treatment

Actinic keratoses are extremely common premalignant keratinocytic neoplastic lesions that develop primarily in fair-complexioned individuals during midlife or beyond. Genetic, occupational and other environmental factors predispose to the development of these lesions. Without treatment, a significant number may progress to fully developed neoplasms, especially squamous cell carcinoma, over a period of 20 to 50 years. The multistep theory of carcinogenesis is helpful in understanding the pathogenesis and progression of this important and highly prevalent lesion.     

Intravascular coagulation. 1. Differential diagnosis and conditioning mechanisms

Intravascular coagulation is an acquired thrombohemorrhagic disorder that occurs as a secondary phenomenon in various medical conditions, usually in patients who are seriously ill. It may occur as an acute fulminant disorder with massive bleeding or thrombosis but more commonly is subacute or chronic. Bleeding may be a prominent feature, or hemostatic abnormalities may be demonstrable only by testing.