TRH on rat conditioned avoidance behavior: interaction with brain catecholamines

TRH (10 micrograms) intracerebroventricularly injected improves the acquisition of a two-day avoidance conditioning. This effect is partially antagonized by pretreatment IP with alpha-methyltyrosine (60 mg/kg) or disulfiram (300 mg/kg). L-DOPA (100 mg/kg) administered IP 2 hr after alpha-MT partially restores the facilitatory effect of the hormone. The possible roles of brain catecholamines on the behavioral effect of TRH are analysed. Other tentative mechanisms of action are also discussed.     

Corticotropin-releasing factor: effect on cerebral blood flow in physiologic and ischaemic conditions

The expression of corticotrophin-releasing factor (CRF) receptors in cerebral arteries and arterioles suggests that CRF may modulate cerebral blood flow (CBF). In the present study, the effects of CRF, CRF-like peptides and the CRF broad spectrum antagonist DPhe-CRF on CBF have been investigated under normal physiologic conditions and in the margins of focal ischaemic insult. The experiments were carried out in anaesthetised and ventilated rats. Changes in CBF after subarachnoid microapplication of CRF and related peptides were assessed with a laser-Doppler flowmetry (LDF) probe. In the ischaemic animals, agents were injected approximately 60 minutes after permanent middle cerebral artery occlusion (MCAo). Microapplication of CRF and related peptides in normal rats into the subarachnoid space produced sustained concentration-dependent increases in CBF. This effect was attenuated by co-application with DPhe-CRF, which did not alter CBF itself. A second microapplication of CRF 30 min after the first failed to produce increases in CBF in normal animals. Microapplication of CRF in the subarachnoid space overlying the ischaemic cortex effected minor increases in CBF whereas D-Phe-CRF had no significant effect on CBF. Activation of the CRF peptidergic system increases CBF in the rat. Repeated activation of CRF receptors results in tachyphylaxis of the vasodilator response. CRF vasodilator response is still present after MCAo in the ischaemic penumbra, suggesting that the CRF peptidergic system may modulate CBF in ischaemic stroke.     

Excessive daytime sleepiness in myotonic dystrophy.

The aim of the present study was to assess whether or not there is any correlation between magnetic resonance imaging (MRI) abnormalities and excessive daytime sleepiness (EDS) in a consecutive series of patients with myotonic dystrophy (MD). The influences of nocturnal breathing abnormalities and sleep morphology on EDS were also evaluated. Ten MD patients were studied by means of an all-night polysomnographic recording, the multiple sleep latency test (MSLT) and MRI. Diagnosis of MD was established on the basis of the clinical and electrophysiological evidence of myotonia as well as of the characteristic genetic pattern. No patient had respiratory failure. Polysomnography and MSLT were also evaluated in ten healthy age-matched controls under the same environmental conditions. The mean MSLT value was significantly lower in patients than in controls. Five of the ten patients were found to have pathological EDS. The quantitative sleep variables and the nocturnal apnoeas in these five patients were not significantly different from those of the patients without EDS. As two patients did not undergo MRI because of claustrophobia, the MRI data were considered in eight patients. Corpus callosum (CC) atrophy was detected in four patients, whereas three patients showed hyperintense areas in the white matter. No correlation was found between EDS and MRI indexes of subcortical atrophy as well as volume of the hyperintense areas. By contrast, a correlation was found between the MSLT value and the reduction in the anterior area of the CC. Our data suggest that CC atrophy might occur in MD patients, and that the size of the CC anterior area might be associated with EDS.     

Occlusion of the extracranial internal carotid artery in the acute stroke; angiographic findings within 6 hours

We studied by angiography 80 patients within 6 hours from the onset of symptoms of supratentorial ischaemic stroke. Occlusion of the internal carotid artery in the extracranial segment was found in 19 patients, at the bifurcation in 11 and at the cervical level in 8. While in the chronic phase of stroke, internal carotid artery occlusion in the cervical segment is an uncommon angiographic finding, we found a high frequency of occlusion at this level (8 out of 19) in our patients. Cervical segment occlusion may be due to a dissecting aneurysm or to an intracranial carotid artery occlusion (embolic or atherothrombotic) with subsequent migration of the clot down to this level. A direct embolic occlusion may be postulated as well.     

Early collateral blood supply and late parenchymal brain damage in patients with middle cerebral artery occlusion

We angiographically studied 80 patients within 6 hours after the onset of ischemic supratentorial infarction. From this group we selected 36 patients with middle cerebral artery occlusion who survived. In these 36 patients, we compared the presence of a collateral blood supply during the early phase with the extent of final parenchymal brain damage obtained by computed tomography 3 months after the event. The presence of a collateral circulation during the first few hours after the stroke reduced the size of the final parenchymal brain damage in patients with middle cerebral artery stem-trunk occlusion. The collateral blood supply was more efficient in patients who had no significant stenosing lesions of the extracranial internal carotid artery. Our data confirm that the lenticulostriate arteries are end arteries not supplied by collateral blood vessels and suggest that lesions formerly thought to be caused by hemodynamic mechanisms (watershed infarcts) or arteriolar lesions (lacunar infarcts) may be due to middle cerebral artery occlusions.