Thalamic astrocytic hamartoma and associated meningoangiomatosis in a German shepherd dog.

The present paper describes an astrocytic thalamic hamartoma associated with tectal meningoangiomatosis in a 3-month-old female German shepherd dog showing strabismus, opistotonus, circling, and fore limb hypermetria. MR images of the brain showed a well-defined intra-axial mass in the tectal region. The mass was hypointense to gray matter on T2-weighted images and hyperintense to gray matter on precontrast T1-weighted images. Histologically, glial cells arranged in a multinodular pattern characterized the mass. More caudally the lesion merged with subpial abnormal newly formed plaque-like shaped tissue characterized by thick branching bundles of spindle-shaped cells surrounding a central vessel. In the nodules, GFAP and vimentin were diffusely expressed. In the vascular proliferation Factor VIII-positive reaction was limited to endothelial cells while the remaining spindle-shaped cells were diffusely SMA-positive. The glial nodules did not express lysozyme and MAC387, nor neurofilaments and nestin.

A case of hypertensive encephalopathy with prominent brainstem presentation.

A 39-year-old woman developed severe arterial hypertension associated with brainstem hyperintensity in T2-weighted images and hyperintense lesion in the left basal ganglia. Clinical findings were a sudden loss of consciousness, confusion, nausea, vomiting and headache. Rapid treatment of hypertension resulted in clinical and radiological improvement. Rapid identification and appropriate diagnostics are essential, as prompt treatment usually results in reversal of symptoms; permanent neurologic injury or death can occur with treatment delay.

Prevention of venous thromboembolism after acute ischemic stroke.

Venous thromboembolism (VTE) is a common complication after acute ischemic stroke. When screened by 125I fibrinogen scanning or venography, the incidence of deep-vein thrombosis (DVT) in stroke patients is comparable with that seen in patients undergoing hip or knee replacement. Most stroke patients have multiple risk factors for VTE, like advanced age, low Barthel Index severity score or hemiplegia. As pulmonary embolism is a major cause of death after acute stroke, the prevention of this complication is of crucial importance. Prospective trials have shown that both unfractionated heparin (UFH) and low molecular weight heparin (LMWH) are effective in reducing DVT and pulmonary embolism in stroke patients. Current guidelines recommend the use of these agents in stroke patients with risk factors for VTE. Some clinicians are concerned that the rate of intracranial bleeding associated with thromboprophylaxis may outweigh the benefit of prevention of VTE. Low-dose LMWH and UFH seem, however, safe in stroke patients. Higher doses clearly increase the risk of cerebral bleeding and should be avoided for prophylactic use. Both aspirin and mechanical prophylaxis are suboptimal to prevent VTE. Graduated compression stockings should be reserved to patients with a clear contraindication to antithrombotic agents.

Impaired renal concentrating ability in hypothyroid man.

The renal concentrating ability was studied in ten patients with hypothyroidism and in 15 euthyroid controls. Solute-free water reabsorption was reduced in the patients with myxedema (4.2 +/- 0.3 ml/min: controls 5.8 +/- 0.6 ml/min; p less than 0.01). This defect was apparent at high rates of solute excretion, and was associated with enhanced excretion of sodium (p less than 0.01) despite a decreased filtered load (p less than 0.005). The myxedema patients had a modest reduction in maximal urine osmolality (p less than 0.04), which was entirely attributable to the lower values observed in younger patients. The results may be explained best by decreased sodium chloride reabsorption in the ascending limb of Henle's loop and/or diminished permeability of the distal nephron in myxedema.

Impaired renal tubular reabsorption of sodium in hypothyroid man.

The renal response to acute salt loading and to stimuli for rapid sodium conservation was studied in 14 patients with untreated myxedema and in 13 euthyroid control subjects in balance on a 155 mEq. sodium intake. The salt-loading studies reveal urinary excretion of sodium in the myxedema patients within the range of controls despite reductions of 34 per cent in glomerular filtration (p less than 0.001) and 37 per cent in filtered load of sodium (p less than 0.001) in the former group. The capacity to conserve sodium in response to stimuli for rapid sodium conservation [postural change and administration of a supramaximal dose of 9alpha-fluorohydrocortisone (9alpha-F)] was impaired in patients with myxedema. The per cent decrease in sodium excretion during the upright posture in the hypothyroid patients was 28 per cent, less than half that observed in the control subjects, 62 per cent (p less than 0.005). Following administration of 2 mg. of 9 alpha-F the per cent decrease in sodium excretion was less (p less than 0.05) in the hypothyroid patients (50 per cent) than in control subjects (72 per cent). In all studies, baseline sodium excretion was comparable in both groups. Fractional excretion of sodium was significantly increased in the hypothyroid patients prior to (p less than 0.005) and during saline loading (p less than 0.05) and at the time of the subnormal responses to stimuli for acute sodium conservation (p less than 0.05 less than 0.005). Potassium excretion was reduced in the hypothyroid patients, even after 9alpha-F. These observations indicate decreased tubular reabsorption of sodium in myxedema under the experimental conditions described. The findings are most consistent with a role for thyroid hormone in normal sodium reabsorption. That this is not related to mineralocorticoid deficiency is suggested by the impaired sodium reabsorptive response to 9alpha-F.