M. Bodosi

Regulation of Brain Water and Electrolyte Contents: The Possible Involvement of Central Atrial Natriuretic Factor

The intraventricular administration of 0.2 or 2 micrograms of synthetic rat atrial natriuretic factor (syn rANF), sequence 101-126 of the precursor, prevented the water accumulation elicited in rat brain by a systemic hypoosmolar fluid load and led to a statistically significant sodium loss from the nervous tissue, while the potassium content remained unaltered. Similar syn rANF administration to rats not treated with a hypoosmolar fluid load caused no significant change in the water, potassium, and sodium content of the hemispheres. In this experiment, a primary systemic action of centrally administered syn rANF with ensuing secondary changes in brain ion and water homeostasis seems unlikely, as the serum osmolality and sodium and potassium concentrations remained unaltered. Thus, a central influence of the intraventricularly administered hormone upon the water and ion balances of the nervous tissue can be hypothesized. The significant loss of sodium may reflect the primary role of volume regulation of the nervous tissue, i.e., the loss of extracellular osmols such as Na+ in response to a hypoosmolar environment. These data lend further support to the concept that a central neuroendocrine system regulates brain ion and volume homeostasis. The possible role of ANF in the management of brain edema should be considered.

Measurements of regional cerebral blood flow and blood flow velocity in experimental intracranial hypertension: infusion via the cisterna magna in rabbits.

Cerebral blood flow velocity, as measured in the intracranial segment of the internal carotid artery by transcranial Doppler sonography via the transorbital route, and regional cerebral blood flow and volume in corresponding cortical areas, as measured by the hydrogen clearance technique, were recorded for eight New Zealand White rabbits subjected to infusion via the cisterna magna to elevate intracranial pressure. In the lower range of autoregulation, that is, at perfusion pressures between 80 and 40 mm Hg and even lower, the changes in cerebral blood flow velocity and cerebral blood flow showed a strong correlation (0.86) under conditions of standard pCO2 (PaCO2 = 35 +/- 2 mm Hg). Autoregulation was exhausted at 40 mm Hg, and the cerebrovascular resistance was minimal. Below this perfusion pressure, the cerebral blood flow and volume dropped sharply, whereas the cerebrovascular resistance gradually increased, indicating that, despite the maximally dilated resistance vessels, intracranial hypertension causes vascular resistance to increase, possibly via blocking of the venous outflow. Our results confirmed that noninvasive and easily (even at bedside) applicable measurements of changes in cerebral blood flow velocity could be a substitute for the cumbersome and expensive isotope measurements of cerebral blood flow in patients with intracranial hypertension.

Increased Concentration of Atrial Natriuretic Factor in the Cerebrospinal Fluid of Patients with Aneurysmal Subarachnoid Hemorrhage and Raised Intracranial Pressure

Plasma and cerebrospinal fluid (CSF) atrial natriuretic factors/peptides (ANFs/ANPs) were measured in 26 patients with normal or raised intracranial pressure (ICP) by means of an instant radioreceptor assay. All 26 patients were suffering from aneurysmal subarachnoid hemorrhage (SAH), and 11 had also developed raised ICP (ICP greater than 20 mm Hg). In SAH patients with normal ICP, the plasma levels of ANF were 20 to 200 pg/ml (mean +/- SE, 89 +/- 68 pg/ml); in the 11 SAH patients with raised ICP, however, ANF levels were 14 to 262 pg/ml (mean 114 +/- 79 pg/ml). The difference was not statistically significant. The ANF/ANP plasma levels in 6 healthy volunteers were 15 to 167 pg/ml (mean 77 +/- 32 pg/ml). Although the ANF/ANP concentration in the CSF of patients with normal ICP did not reach the lower limit of detectability (i.e., 4 pg/ml) in any case, in those with elevated ICP it was 14 to 120 pg/ml (mean 49 +/- 37 pg/ml). This difference was statistically highly significant. The results of this preliminary study suggest that the ANF/ANP concentration in human CSF is 1 to 2 orders lower than that in the plasma and that there is no significant correlation between ANF/ANP levels in the CSF and the plasma. After SAH in patients with raised ICP, there was an accompanying increase in the ANF/ANP concentration in the CSF, but the ANF/ANP concentration in the plasma was not changed significantly. Accordingly, a central ANF/ANP release might be hypothesized to play a causative or adaptive role in the neuroendocrine regulation of ICP dynamics, although this may simply be an epiphenomenon.

Significance of the Rate of Systemic Change in Blood Pressure on the Short-Term Autoregulatory Response in Normotensive and Spontaneously Hypertensive Rats

Cerebral autoregulation, the physiological regulatory mechanism that maintains a constant cerebral blood flow (CBF) over wide ranges of arterial blood pressure, was investigated in normotensive and spontaneously hypertensive rats by means of laser-Doppler flowmetry. Systemic arterial hypertension was produced at rates ranging from 0.02 mm Hg/second to 11 mm Hg/second by constant infusion of epinephrine and norepinephrine. Systemic arterial hypotension was produced at rates ranging from -0.03 mm Hg/second to -12 mm Hg/second, either by bleeding the animals into a reservoir or by compressing the abdomen. In those cases with a low rate of change in systemic arterial blood pressure (SABP), the measurements lasted for 5 +/- 2 minutes, and in those with a high rate of change in SABP, measurements lasted for 40 +/- 30 seconds. The purpose was to record the time of onset and course of autoregulation in the basal ganglia in response to slow or rapid changes in SABP. CBF in the basal gray matter remained at baseline values (i.e., autoregulation was functioning) if the rate of increase of SABP did not exceed a critical value (0.10 mm Hg/second in the normotensive rats; 0.35 mm Hg/second in the spontaneously hypertensive rats). When hypertension was produced at faster rates, CBF followed arterial blood pressure passively, and no autoregulatory response was observed for 2 +/- 1 minutes. Hypotension did not change the baseline CBF when it was not produced at a rate faster than -0.4 mm Hg/second in normotensive rats and -0.15 mm Hg/second in spontaneously hypertensive rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Use of Transcranial Doppler Sonography and Acetazoalmide Test to Demonstrate Changes in Cerebrovascular Reserve Capacity Following Carotid Endarterectomy

OBJECTIVES To assess the effect of carotid endarterectomy on cerebrovascular reserve capacity. METHODS Cerebral blood flow velocity (CBFV) and cerebrovascular reserve capacity (CVRC) were measured by transcranial Doppler sonography (TCD) and acetazolamide test in 40 patients who underwent uncomplicated unilateral carotid endarterectomy (CEA). Indication for operation was limited to stenoses > 70% as documented by angiography and/or Duplex scanning. The TCD studies were carried out 6 days (range 1-14 days) before and 8 days (range 5-12 days) after endarterectomy. RESULTS Before endarterectomy, resting CBFV values and CVRC in the 40 patients were significantly different between the operated (51 +/- 19 cm/s; 20 +/- 16%) and the non-operated (60 +/- 19 cm/s; 34 +/- 24%) hemisphere (p < 0.05;p < 0.01). After CEA the overall increase of resting CBFV of the operated side was highly significant with preoperative CBFV values of 51 +/- 19cm/s and postoperative values of 62 +/- 15 cm/s (p < 0.01). Cerebrovascular reserve capacity after operation was increased on both sides significantly (non-operated side: from 34 +/- 24% to 43 +/- 19%, p < 0.05; operated side: from 20 +/- 16% to 51 +/- 18%, p < 0.001), and the preoperative asymmetry was no longer present. CONCLUSIONS CEA has a beneficial effect on the cerebral circulation in most patients, even those who presented with asymptomatic carotid artery stenosis. Since CVRC has been assessed in the early postoperative period, our findings also suggest that cerebral vascular adaption occurs within 2 weeks after CEA.

A report on neurosurgical workforce in the countries of the EU and associated states

SummaryAimAim of this report was to present recently collected data on neurosurgical workforce in the countries of the EU and associated states.MethodsData were obtained from 27 countries by means of a questionnaire developed by members of a working group of the UEMS Section of Neurosurgery (UEMS = Union Europénne des Médecins Spécialistes; European Union of Medical Specialists). Most data originate from 2005/2006. Results were discussed, amended, and approved by the countries’ delegates of the UEMS Section of Neurosurgery.ResultsThe number of Neurosurgeons (NS) per population varies considerably among these countries. The mean is one neurosurgeon per 99,152 population. The number of neurosurgical operations per population per year varies similarly with a mean of 1,642 operations per million population/year. Countries with fewer neurosurgeons per population tend to have less neurosurgical operations per population and vice versa. The average number of operations performed by one neurosurgeon per year (annual caseload) is between 56 and 300 with a mean of 154. A numerus clausus for neurosurgical training is reported in 13 countries, another 13 countries have no numerus clausus. The annual intake of new trainees is between 2.4 and 10.3% of the number of accredited neurosurgeons with a mean of approx. 5.2%. The average yearly loss rate due to retirement, sickness, other activities, etc. can only be estimated and lies in the range between 2.3 and 3.36% of the number of accredited NS. According to the figures provided by the countries, the total number of accredited NS in 2005/2006 was approx. 6,280 for a population of about 504.7 millions. These countries had an annual intake of approx. 332 new trainees.

Venous cerebral infarction due to simultaneous occurrence of dural arteriovenous fistula and developmental venous anomaly.

Summary A case of a left frontal lobe infarction in a 31-year-old male patient is presented. This patient had bilateral frontal dural arteriovenous fistulae (DAVF) and a left frontal developmental venous anomaly (DVA). It is suggested that the simultaneous occurrence of these vascular anomalies was the cause of his infarction.

Influence of nitrovasodilators and cyclooxygenase inhibitors on cerebral vasoreactivity in conscious rabbits

Since the nitric oxide (NO) and cyclooxygenase pathways have been suggested to have important roles in most vasodilations, our aim was to study the influence of cyclooxygenase inhibitors and nitrovasodilators on cerebrovascular reserve capacity. Corticocerebral blood flow was measured by hydrogen polarography during hypercapnia and acetazolamide stimuli in conscious rabbits. The measurements were repeated in the presence of N(omega)-nitro-L-arginine methyl ester (L-NAME) and indomethacin as nitric oxide synthase (NOS) and cyclooxygenase inhibitors. The effects of nitroglycerin and isosorbide-5-nitrate were also tested. L-NAME completely, while indomethacin markedly inhibited the hypercapnic corticocerebral blood flow response. Nitroglycerin and isosorbide-5-nitrate significantly attenuated hypercapnia elicited corticocerebral blood flow increase. The different treatments reduced only moderately the acetazolamide-induced corticocerebral blood flow response. These results lend support to the hypothesis that antithrombotic and antiinflammatory medication (cyclooxygenase inhibitors) and nitrovasodilator treatments could interfere with the measurement of cerebrovascular reactivity resulting in underestimation of the cerebrovascular reserve capacity in patients taking these drugs.

Central neuroendocrine control of the brain water, electrolyte, and volume homeostasis.

In 1981 Marcus Raichle put forward the hypothesis that a central neuroendocrine system regulates the brain ion and water homeostasis38. In this presentation I would like to summarize briefly the available data—including our own results—in support of this hypothesis. The hypothesis supposes that three cell groups (brain capillary endothelial cells, secretory cells of the choroid plexus, and astroglia) regulate the internal ionic environment of the brain38. A unique element of this hypothesis is that the regulation of the ion and volume homeostasis of the brain is orchestrated by a central neuroendocrine system capable of affecting all three cell types38.

Intraventricular hemorrhage as a false localizing sign of a thoracolumbar arteriovenous malformation: case report

BACKGROUND Spinal arteriovenous malformation (SAVM) is a relatively rare disease characterized by a high incidence of intramedullary and subarachnoid haemorrhage. When the hemorrhage is profuse and the SAVM is in the cervical region the symptoms (disturbance of consciousness, papilledema, cranial nerve palsies, and convulsions) may be so severe and rapid in their onset that they may be mistaken for intracranial hemorrhage. We report here on a patient with a SAVM at T10-12, which bled intracranially, mainly intraventricularly, and resulted first in respiratory arrest and unconsciousness. CASE DESCRIPTION The patient had been well until he was 28 years old when, during intercourse, he suffered a terrible headache and suddenly lost consciousness, with a transient respiratory arrest. He was also noted to have right hemiparesis. A computed tomography scan demonstrated intraventricular hemorrhage. After a 24-hour period of artificial ventilation the patient regained consciousness and the right arm paresis completely recovered, but a gradual worsening of the motor function of the left leg developed. Digital subtraction angiography did not demonstrate any intracranial source of bleeding, whereas spinal angiography revealed a SAVM located at the medullary cone, which was totally removed by surgery. CONCLUSION The case reported here raises several important issues. First, the advisability of spinal magnetic resonance imaging in the investigation of intraventricular (and subarachnoid) hemorrhage in patients with no demonstrable intracranial source. Secondly, the benefits of early diagnosis and reestablishment of the spinal cord circulation before the onset of thrombosis and the progressive phase of myelopathy. Finally, the necessity of complete obliteration and treatment of SAVMs even in patients with fixed neurologic deficits, because rebleeding of lower thoracic or lumbar SAVMs can lead to impairment at a higher level with severe or lethal consequences.