Search

A 75-year-old woman presented to her local endocrine service with tiredness, palpitations, and enlargement of a longstanding goitre. Unexpectedly, her thyrotropin (thyroid-stimulating hormone [TSH]) concentration was not suppressed (6·3 mU/L; reference range 0·35–5·5) despite raised concentrations of thyroid hormones (free thyroxine [T$_{4}$] 89·1 pmol/L [reference range 10–19·8]; free triiodothyronine [T$_{3}$] 11·7 pmol/L [3·0–6·5]). After exclusion of laboratory assay interference, a thyrotropin-releasing hormone test showed an attenuated response (TSH at 0 min was 6·1 mU/L, at 20 min was 6·8 mU/L, and at 60 min was 8·5 mU/L), raising suspicion of a thyrotropinoma (also known as TSHoma). However, pituitary MRI was normal. The patient was referred to our centre for further assessment. On repeat MRI, the pituitary gland showed mild asymmetry (right larger than left; figure A). Functional imaging with 11C-methionine ($^{11}$C-Met) PET-CT revealed intense tracer uptake (denoting active peptide synthesis) on the right side of the sella (red hot spot in figure A). Treatment with a depot somatostatin analogue (SSA) led to resolution of symptoms and normalisation of thyroid function (TSH 0·6 mU/L, free T$_{4}$ 12·5 pmol/L, and free T$_{3}$ 3·8 pmol/L). Repeat $^{11}$C-Met PET-CT showed absence of the right-sided focal hot spot (figure B). 14 months into treatment, the patient had several hypoglycaemic episodes, which resolved after discontinuation of SSA. However, thyrotoxicosis recurred (TSH 4·3 mU/L, free T$_{4}$ 38·1 pmol/L, free T$_{3}$ 11·6 pmol/L), and repeat $^{11}$C-Met PET-CT revealed the reappearance of the right-sided hot spot (figure C). During pituitary surgery, a microthyrotropinoma was resected from the right side of the gland (figure D). The patient remains in clinical and biochemical remission more than 12 months after surgery and has normal pituitary function.

Computed tomography is currently the standard diagnostic tool for the evaluation of the skull base. The complex anatomy of this area is the primary reason why planar bone scintigraphy is often unsatisfactory; exact localization of abnormalities may be very difficult. These limitations may be overcome by SPECT. Seventeen patients with clinical features of basal skull involvement were assessed by CT, SPECT, and planar scintigraphy. Subsequent clinical diagnoses were malignancy in 15 patients, vasculitis in 1 patient, and osteomyelitis in 1 patient. Computed tomography with IV contrast was performed through the skull base at 5 mm intervals. Planar scintigraphy with Tc-99m MDP was followed by SPECT. Bony involvement compatible with the clinical findings was demonstrated by CT scans in 6 patients, by planar scintigraphy in 7 patients, and by SPECT in 9 patients. The abnormalities that were identified by CT were all identified by SPECT. This study suggests that, in imaging the skull base, SPECT is more sensitive and provides better anatomical localization than planar imaging and appears useful in patients with a negative CT study.

OBJECTIVE: To characterize and quantify the patterns of temporal lobe atrophy in AD vs semantic dementia and to relate the findings to the cognitive profiles. Medial temporal lobe atrophy is well described in AD. In temporal variant frontotemporal dementia (semantic dementia), clinical studies suggest polar and inferolateral temporal atrophy with hippocampal sparing, but quantification is largely lacking. METHODS: A volumetric method for quantifying multiple temporal structures was applied to 26 patients with probable AD, 18 patients with semantic dementia, and 21 matched control subjects. RESULTS: The authors confirmed the expected bilateral hippocampal atrophy in AD relative to controls, with involvement of the amygdala bilaterally and the right parahippocampal gyrus. Contrary to expectations, patients with semantic dementia had asymmetric hippocampal atrophy, more extensive than AD on the left. As predicted, the semantic dementia group showed more severe involvement of the temporal pole bilaterally and the left amygdala, parahippocampal gyrus (including the entorhinal cortex), fusiform gyrus, and the inferior and middle temporal gyri. Performance on semantic association tasks correlated with the size of the left fusiform gyrus, whereas naming appeared to depend upon a wider left temporal network. Episodic memory measures, with the exception of recognition memory for faces, did not correlate with temporal measures. CONCLUSIONS: Hippocampal atrophy is not specific for AD but is also seen in semantic dementia. Distinguishing the patients with semantic dementia was the severe global but asymmetric (left > right) atrophy of the amygdala, temporal pole, and fusiform and inferolateral temporal gyri. These findings have implications for diagnosis and understanding of the cognitive deficits in AD and semantic dementia.

The management of unruptured intracranial aneurysms requires knowledge of the natural history of these lesions and the risks of repairing them.A total of 2621 patients at 53 participating centers in the United States, Canada, and Europe were enrolled in the study, which had retrospective and prospective components. In the retrospective component, we assessed the natural history of unruptured intracranial aneurysms in 1449 patients with 1937 unruptured intracranial aneurysms; 727 of the patients had no history of subarachnoid hemorrhage from a different aneurysm (group 1), and 722 had a history of subarachnoid hemorrhage from a different aneurysm that had been repaired successfully (group 2). In the prospective component, we assessed treatment-related morbidity and mortality in 1172 patients with newly diagnosed unruptured intracranial aneurysms.In group 1, the cumulative rate of rupture of aneurysms that were less than 10 mm in diameter at diagnosis was less than 0.05 percent per year, and in group 2, the rate was approximately 11 times as high (0.5 percent per year). The rupture rate of aneurysms that were 10 mm or more in diameter was less than 1 percent per year in both groups, but in group 1, the rate was 6 percent the first year for giant aneurysms (or =25 mm in diameter). The size and location of the aneurysm were independent predictors of rupture. The overall rate of surgery-related morbidity and mortality was 17.5 percent in group 1 and 13.6 percent in group 2 at 30 days and was 15.7 percent and 13.1 percent, respectively, at 1 year. Age independently predicted surgical outcome.The likelihood of rupture of unruptured intracranial aneurysms that were less than 10 mm in diameter was exceedingly low among patients in group 1 and was substantially higher among those in group 2. The risk of morbidity and mortality related to surgery greatly exceeded the 7.5-year risk of rupture among patients in group 1 with unruptured intracranial aneurysms smaller than 10 mm in diameter.