Histopathologic analysis of foci of signal loss on gradient-echo T2*-weighted MR images in patients with spontaneous intracerebral hemorrhage: evidence of microangiopathy-related microbleeds.

BACKGROUND AND PURPOSE: Patients with spontaneous intracerebral hemorrhage (ICH) frequently have small areas of signal loss on gradient-echo T2*-weighted MR images, which have been suggested to represent remnants of previous microbleeds. Our aim was to provide histopathologic support for this assumption and to clarify whether the presence and location of microbleeds were associated with microangiopathy. METHODS: We performed MR imaging and correlative histopathologic examination in 11 formalin-fixed brains of patients who had died of an ICH (age range, 45-90 years). RESULTS: Focal areas of signal loss on MR images were noted in seven brains. They were seen in a corticosubcortical location in six brains, in the basal ganglia/thalami in five, and infratentorially in three specimens. Histopathologic examination showed focal hemosiderin deposition in 21 of 34 areas of MR signal loss. No other corresponding abnormalities were found; however, hemosiderin deposits were noted without MR signal changes in two brains. All specimens with MR foci of signal loss showed moderate to severe fibrohyalinosis, and there was additional evidence of amyloid angiopathy in two of those brains. CONCLUSION: Small areas of signal loss on gradient echo T2*-weighted images indicate previous extravasation of blood and are related to bleeding-prone microangiopathy of different origins.

Brain-stem auditory evoked potential monitoring. Variations of stimulus artifact in brain death.

Brain-stem auditory evoked potentials (BAEPs) were recorded in 20 subjects with brain death (mean age, 33.2 +/- 15.1 years) and 20 healthy volunteers (mean age, 29.8 +/- 6.8 years). Brain death was due to head injury (n = 14), encephalitis (n = 3), brain-stem hemorrhage (n = 1), cerebellar hemorrhage (n = 1) or cerebral infarction (n = 1). The presence, latency and amplitude of the individual BAEP components and variations of the stimulus artifact were evaluated. The mean (+/- S.D.) amplitude of the stimulus artifact was 0.26 +/- 0.12 microV in the brain-dead subjects and 0.09 +/- 0.05 microV in the control group (P < 0.001, t test). The causes of the phenomenon of increasing stimulus artifacts in the evolution of brain death remain unclear.

Plasma levels of parathyroid hormone-related peptide are elevated in hyperprolactinemia and correlated to bone density status.

Osteopenia is an important clinical manifestation of hyperprolactinemia. Bone loss in these patients has mainly been attributed to concomitant deficiency of gonadal hormones rather than to hyperprolactinemia per se. Parathyroid hormone-related peptide (PTHrP) is expressed in human mammary tissue, and elevated circulating PTHrP levels as well as concomitant hypercalcemia have been described during lactation. We sought to determine circulating PTHrP levels in patients with long-standing hyperprolactinemia and whether PTHrP may exert possible systemic effects on bone and mineral metabolism. We studied 45 patients (30 women and 15 men) with persisting hyperprolactinemia 6 +/- 4 years (mean +/- SD) after trans-sphenoidal surgery for prolactin-producing pituitary adenomas. PTHrP levels in 117 healthy controls were 10.6 +/- 7.3 pmol-eq/l (mean +/- SD). In hyperprolactinemic patients, plasma PTHrP was elevated to 30.3 +/- 13.4 pmol-eq/l (p < 0.001, n = 45), and in patients with humoral hypercalcemia of malignancy PTHrP levels were 52.9 +/- 29.6 (p < 0.001 to controls and hyperprolactinemic patients). Fifty-three percent of hyperprolactinemic patients (n = 24) had clearly elevated PTHrP levels (> 2 SD). Retrospective immunocytochemical studies of the removed pituitary adenomas from 19 patients generally showed a higher degree of immunoreactivity for PTHrP (1-34) in all but one case when compared with normal pituitary tissue. Patients with elevated circulating PTHrP levels showed in most instances strong immunoreactivity to PTHrP in 70-100% of tumor cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Interstitial 1.06 Nd:YAG laser thermotherapy for brain tumors under real-time monitoring of MRI: experimental study and phase I clinical trial.

This paper presents the experimental and clinical results of interstitial 1.06 Nd:YAG laser thermotherapy (ILTT) for brain tumors under real-time monitoring by magnetic resonance imaging. The authors chose a laser heat source for interstitial thermotherapy of brain tumors for several important reasons: (1) Laser heat delivery is less complicated and more controlled; (2) laser effects on tissue can be tested, monitored, and controlled by MRI. A 1.064 nm Nd:YAG laser and a specially designed laser optic fiber (ILTT) were used in C.W. mode this study. The laser was used at 4 W at a C.W. mode pulse and total exposure duration was 10 minutes (total energy was 2400 joules). Temperature distribution was determined with a microprocessor-based thermometer and by the levels of the signal intensity under MRI. The relationship between the temperature and MRI signal intensity allowed exploration of the possibility of using MRI as a noninvasive temperature monitoring method. Two patients with glioblastoma and one patient with a brain metastasis were treated with this modality. The results and indications are presented and discussed.

Brain neurotransmitter changes in three patients who had a fatal hyperthermia syndrome.

The authors examined the autopsied brains from three patients who had a fatal hyperthermia syndrome. There was marked hypothalamic noradrenaline depletion in all three patients, severe brain choline acetyltransferase deficiency with nucleus basalis cell loss in two patients, and mild to moderate brain choline acetyltransferase loss in one patient. Striatal dopamine metabolite/dopamine ratio was below normal in two patients and not elevated, as would be expected after short-term neuroleptic administration, in the third. This suggests that reduced capability (aggravated by the cholinergic deficit) of the nigrostriatal dopamine system to respond adequately to stress and/or neuroleptic-induced receptor blockade may be important in the development and course of fatal hyperthermia syndrome.