Brain metabolism after recurrent insulin induced hypoglycaemic episodes: a PET study.

Neuropsychological testing was carried out and the rate of oxygen metabolism in the brain was measured by PET in 15 highly selected patients with type 1 diabetes. The aim was to investigate the impact on the brain of hypoglycaemic comas resulting from insulin treatment. No significant difference was found between nine patients with a history of more than 10 hypoglycaemic comas and six others who denied any history of such events. These data suggest that intensified insulin treatment, although increasing the frequency of hypoglycaemic coma, may not always be harmful for the brain. This may be explained by the limited duration of hypoglycaemic coma induced by conventional insulin treatment.

Cerebral infarction due to painless thoracic aortic and common carotid artery dissections.

BACKGROUND: Aortic arch dissection is usually lethal unless emergency surgery is performed. The dissection rarely may have a benign outcome or may occur without pain and be revealed by cerebral infarction. It is then likely to be seen primarily by a neurologist. In such cases, the value of new noninvasive diagnostic testing has not been reported. CASE DESCRIPTION: A 51-year-old man had a sudden left-sided hemiplegia due to hemorrhagic capsular and caudate infarcts on the right side. Cervical ultrasound examination with color flow imaging showed a bilateral common carotid artery dissection extending up to the bifurcation. Transesophageal echocardiography showed an aortic arch dissection, involving the innominate and left common carotid artery origins, which was confirmed by magnetic resonance imaging and aortography. The patient spontaneously fully recovered and is still alive 24 months after the stroke onset. CONCLUSIONS: This case emphasizes the usefulness of new noninvasive techniques such as transesophageal echocardiography and color-coded Doppler echocardiography in the diagnosis and follow-up of painless dissection of aortic and common carotid arteries. This cause of stroke may be underestimated.

[Benign cerebral angiopathies and phenylpropanolamine]. / Angiopathies cérébrales bénignes et phénylpropanolamine.

Heroin, cocaine, amphetamines, sympathomimetic drugs can cause cerebral angiopathy. We report 2 patients with cerebrovascular disorders after ingestion of a nasal vasoconstrictor containing phenylpropanolamine (P.P.A.). The first patient had two acute repetitive attacks of severe headache and vomiting, occurring after a daily treatment with 180 mg of P.P.A. during 6 weeks. The second patient had an intracerebral hemorrhage, occurring some hours after taking for the first time 120 mg of P.P.A. In both cases, cerebral angiography, performed in the next week, demonstrated segmental narrowing and dilatations of medium-size intracranial arteries. None of the usual causes of cerebral vasculitis were present. The outcome was favorable and follow-up angiograms showed the disappearance of the beading pattern. P.P.A. is widely used over the counter in diet pills and stimulants. Cerebral vascular complications have been rarely reported, always hemorrhagic and often associated with cerebral vasculitis. They are unrelated to duration or dosage of treatment. The mechanism is unclear but could result from several factors: chronic or paroxystic high blood pressure, immuno-allergic vasculitis, arterial spasm, direct "toxic" effect of the P.P.A. on the arterial wall may be increased by other drugs and caffeine.

[Neurological manifestations of Behçet's disease]. / Les manifestations neurologiques de la maladie de Behçet.

Characterised classically by the association of buccal and genital ulceration and uveitis with hypopyon, Behçet's disease has many other manifestations, amongst which the neurological ones (often referred to as Neuro-Behçet) are important in view of their frequency and their gravity. Anatomically, it produces a subacute haemorrhagic and necrotising meningo-encephalitis, which most typically effects the hypothalamus and brainstem. Clinically, there is extreme polymorphism, central manifestations being the most frequent: seizures, organic brain syndromes, disorders of consciousness, aphasia, hemiplegia, cranial nerve palsies, pseudobulbar and extrapyramidal syndromes and meningism. The peripheral nerves and muscles are rarely affected. Alongside Neuro-Behçet per se, attention has recently been directed to the various cerebro-vascular manifestations, dominated by venous thrombosis. A review of the principal neurological manifestations is given, with comment on anatomico-pathological aspects, clinical presentation, investigational techniques, diagnostic difficulties, prognosis, and treatment.

[Role of electroencephalography in the diagnosis of acute cerebral diseases]. / Place de l'électroencéphalogramme dans le diagnostic des affections cérébrales aiguës.

It appears from a study of 100 cases of acute cerebral disease that electroencephalography is valuable as part of the diagnosis strategy and not only to establish the correct final diagnosis. This examination therefore plays a non-negligible role in neurological practice. In a number of diseases it provides information that no other examination can provide, being a dynamic, functional method of brain tissue analysis.

Cephalic magnetic resonance imaging of boxers. Preliminary results.

A prospective study of 52 boxers, 20-60 years, 13 of them amateurs and 39 professionals, has been made using magnetic resonance imaging (MRI) at 0.15 T. Twelve of the boxers were still active, while the other 40 had retired after about 10 years of boxing. Multi-slices in two planes without gap were performed using T1 and T2 weighted sequences. The findings were correlated to the number of matches, the number of knock outs, the severity of head trauma, the style of the boxer, and to the clinical findings and the findings at EEG. There was a good correspondence between the presence of lesions and the style of the boxer. The changes noted--mainly atrophic--occurred among those with capacity to 'stand punishment'. MRI offers an opportunity to evaluate the effect of trauma and the information obtained may be used to prevent disabilities among boxers.

[Chloroquine neuromyopathies: 4 cases during antimalarial prevention]. / Neuromyopathies à la chloroquine: 4 cas au cours d'une prophylaxie anti-paludéenne.

Four cases of chloroquine neuropathy presented two points of particular interest: 1) these were all young women with strictly prophylactic doses of chloroquine (100 mg/24 h); two patients showed pronounced loss of weight; 2) signs of myogenic lesions were apparent in only one patient whereas clinical and electric signs of neurogenic involvement were observed in all 4 cases. Biopsy in 3 patients (muscle in one and muscle and nerve in two) failed to show characteristic vacuoles; in one case mild segmental demyelinization was present. A favorable course was obtained in all cases after discontinuation of chloroquine, with dramatic recovery from the motor deficit. Pharmacokinetic studies in 1 patient showed abnormally high chloroquine levels at initial assay with slow elimination after its discontinuation.

Renal mercury content in HgCl2-induced acute renal failure in furosemide/saline-protected and nonprotected rats.

Renal mercury content, urinary mercury excretion and renal function were studied in rats with acute renal failure (ARF) induced by subcutaneous injection of 2, 3, 6, or 10 mg/kg HgCl2. Similarly poisoned rats were protected against ARF by continuous intravenous infusion of furosemide and saline. Excellent protection was obtained in rats receiving 2,3, and 6 mg/kg HgCl2, whilst some animals developed moderate azotemia after 10 mg/kg HgCl2. Renal mercury content 48 h after HgCl2 injection did not differ appreciably between protected and nonprotected groups of rats and showed no relation to the dose of HgCl2 injected or to the degree of renal failure. Urinary Hg excretion was variable during the first 24 h after HgCl2 injection and tended to be higher with higher dosage unless the animals became anuric early on. Hg excretion during the second 24 h was independent of dosage, but was comparatively high in functionally well protected rats and low in oliguric animals with severe renal failure. Attempts at detoxication with the potent chelating agent complexon I after 6 mg/kg HgCl2 failed completely: Renal mercury content was similar to that in the other groups of rats and every single rat so treated developed severe anuric renal failure. Although dose-dependent functional injury after HgCl2 may be related to the amount of Hg reaching the kidney during the initial phase, we have to conclude that HgCl2 toxicity is unrelated to the amount of Hg found in renal tissue at 48 h. Furthermore, furosemide/saline protection does not act through increasing urinary Hg excretion or decreasing the amount of toxin accumulating in renal tissue.

Local cerebral glucose utilisation in treated and untreated patients with Parkinson's disease.

Using the 18f-fluoro-2-deoxy-d-glucose technique and positron emission tomography (PET), the local cerebral glucose utilisation (1CMRGlc) was measured in four non-demented patients with early-onset, bilateral Parkinson's disease characterised by the predominance of akinesia. The study was done twice, first in the untreated condition, and then after levodopa had been resumed. Despite a marked clinical improvement, we found no alteration in 1CMRGlc between the first and second studies in any of the brain structure analysed. Compared to control values, 1CMRGlc in the basal ganglia was moderately increased in both studies. These essentially negative findings agree with most previous human or animal studies, and indicate that the functional alterations in the central dopaminergic systems of patients with Parkinson's disease have metabolic correlates that are too small to be demonstrated by current PET devices.

Local interrelationships of cerebral oxygen consumption and glucose utilization in normal subjects and in ischemic stroke patients: a positron tomography study.

With the use of positron emission tomography (PET) and the 15O steady-state-[18F]fluorodeoxyglucose combined method, the local interrelationships between the cerebral metabolic rate for oxygen (CMRO2) and the cerebral metabolic rate for glucose ( CMRGlc ) were investigated in control subjects and in stroke patients. In addition to the classic in vivo autoradiographic approach, a kinetic method was used to measure CMRGlc because it was expected to be more reliable in cerebral ischemia. In control subjects local coupling between CBF, CMRO2, and CMRGlc was confirmed, and acceptable values for the CMRO2/ CMRGlc ratio were found; the latter, however, was lower in white matter than in gray. Uncoupling between CMRO2 and CMRGlc was observed in all stroke patients, suggesting that (1) enhanced anaerobic glycolysis occurred both in reperfused recent infarcts and in chronically ischemic tissue, and (2) substrates other than blood-borne glucose were being oxidized at the borders of recent infarcts. However, methodological uncertainties presently make such observations only tentative. Finally, a coupled depression of CMRO2 and CMRGlc was found in the contralateral cerebellum.

[Positron emission tomography in the physiopathological study of cerebral ischemia in man]. / Apport de la tomographie par émission de positons dans l'étude physiopathologique de l'ischémie cérébrale chez l'homme.

The development of positron emission tomography now allows the local study of cerebral blood flow, oxygen consumption and glucose utilization in ischemic stroke patients. In recent cerebral infarction, a disruption of the normal couple between flow and metabolism is almost constantly observed: in the first few days cerebral blood flow is either inadequate (persistent ischemia) or over-abundant ("luxury perfusion"), whereas a late "luxury perfusion" is almost constant within the necrotic area between the 10th and the 40th day. Threshold values for cerebral blood flow and oxygen consumption that are ultimately associated with necrosis or tissue integrity have been determined. A metabolic depression without C.T. Scan counterpart has been observed in various brain structures remote from the infarcted area per se. Lastly, the hemodynamic and metabolic effects the superficial-temporal-middle-cerebral-artery anastomosis have been studied.

Tissue acid-base balance and oxygen metabolism in human cerebral infarction studied with positron emission tomography.

Nine patients who had suffered strokes were examined between 10 and 34 days after onset using positron emission tomography. DMO labeled with carbon 11 was used to evaluate brain acid-base balance, and the oxygen-15 inhalation technique was used to measure regional cerebral blood flow, the oxygen extraction fraction, and cerebral metabolic rate for oxygen. [11C]DMO concentration and oxygen metabolism variables were measured in the infarcted area and in the symmetrical region in the contralateral cerebral hemisphere. [11C]DMO concentration was found to be unchanged or slightly increased in five cases and markedly increased in four cases. The apparent increase in tissue pH can be explained by the presence of a large extracellular fluid space with a pH nearly identical to that of brain plasma, or by an increase in intracellular pH, or by both phenomena. The change in [11C]DMO concentration in the infarcted area relative to that in the normal tissue was independent of the change in blood flow. Cerebral metabolic rate for oxygen was decreased in all cases. The increase in [11C]DMO concentration in the infarcted area was linearly correlated with the decrease in the oxygen extraction fraction in the same region; that is, it was correlated with the occurrence of perfusion in excess of metabolic demand. The overabundant local perfusion could play a role in the decreased H+ content.

[Cerebral blood flow and oxygen extraction in lacunar hemiplegia. Semi-quantitative study using oxygen 15 and emission tomography]. / Débit sanguin cérébral et extraction d'oxygène dans les hémiplégies lacunaires. Etude semi-quantitative par l'oxygène 15 et la tomographie d'émission.

The oxygen 15 non invasive continuous inhalation technique coupled with positron emission tomography (P.E.T.) allows the local study of cerebral blood flow and oxygen metabolism. Recent P.E.T. studies have demonstrated the frequent occurrence of widespread metabolic depression remote from the site of middle cerebral artery territory infarct per se, especially over the cortical mantle and thalamus ipsilaterally, and over the cerebellar hemisphere contralaterally. These phenomena have been taken as indicative of transneural depression (i.e. diaschisis). We thought it interesting to study the possible occurrence of such abnormalities in patients with lacunar syndromes. We have applied the (15)0 technique to six patients (2 with pure motor hemiplegia, 4 with ataxic hemiparesis) for whom no large causal ischemic lesion could be demonstrated on CT scans; in only one patient was a lacunar lesion, presumably responsible for the clinical deficit demonstrated. Compared to a set of 19 patients without brain disease, the semi-quantitative results (analyzed in terms of asymmetry indices between homologous brain regions) in our patients did not disclose any pathophysiologically significant abnormality. More specifically, no evidence of physiological dysfunction similar to that reported in internal carotid artery territory infarcts, was detected over the cerebral or cerebellar cortices. These findings are commented upon in view of the presumably small size and the uncertain topography of the causal lesion.

Hgcl2-induced acute renal failure in the rat. Effect of water diuresis, saline loading, and diuretic drugs.

A variety of pretreatment-treatment protocols were applied to rats with ARF induced by the subcutaneous injection of 6 mg of HgCl2 per kilogram body weight. Renin depletion induced by DOCA-saline pretreatment was associated with protection against HgCl2-induced ARF only when the saline diuresis was maintained by drinking 1% NaCl after injury. Twenty-four dehydration followed by free access to tap water annihilated the protective effect of DOCA-saline pretreatment despite maintained depletion of renal renin. Continuous intravenous loading with saline and furosemide, although increasing renal renin levels, afforded as much protection as saline loading alone. Ethacrynic acid, which did not increase salt excretion in our rats, as well as water diuresis, failed to be protective. A loose correlation was found between he amount of histological damage to the convoluted parts of the proximal tubules and the degree of renal functional impairment. Thus protection against HgCl2-induced ARF was independent of the renal renin level but closely related to urinary NaCl excretion after the injury. Saline diuresis could act by relieving or preventing tubular obstruction.

[A 15oxygen positron study of relative local perfusion and oxygen extraction of the brain in lacunar hemiparesis (author's transl)]. / Débit sanguin cérébral et extraction d'oxygène dans les hémiplégies lacunaires. Etude semi-quantitative par l'oxygène-15 et la tomographie d'émission.

The oxygen-15 non-invasive continuous inhalation technique coupled with positron emission tomography (PET) allows the local study of cerebral blood flow and oxygen metabolism. Recent PET studied have demonstrated the frequent occurrence of widespread metabolic depression remote from the site of middle cerebral artery territory infarct per se, especially over the cortical mantle and thalamus ipsilaterally, and over the cerebellar hemisphere contralaterally. These phenomena have been taken as indicative of a transneural depression (i.e. diaschisis). We thought interesting to study the possible occurrence of such abnormalities in patients with lacunar syndromes. We have applied the 15O technique to seven patients (2 with pure motor hemiplegia, 5 with ataxic hemiparesis) in whom no large causal ischemic lesion could be demonstrated on CT Scans; in only one patient was a lacunar lesion, presumably responsible for the clinical deficit, evidenced. Compared to a set of 19 patients without brain disease, the semi-quantitative results (analyzed in terms of asymmetry indices between homologous brain regions) in our patients did not disclose any pathophysiologically significant abnormality. More specifically, no evidence of physiological dysfunction similar to that reported in internal carotid artery territory infarcts, was detected over the cerebral or the cerebellar cortices. These original findings are commented upon in view of the presumably small size and the uncertain topography of the causal lesion.

[Neurologic manifestations of Behcet's disease. 24 cases]. / Manifestations neurologiques de la maladie de Behçet. Vingt-quatre observations.

Dominant symptoms in 24 patients with neurological manifestations of Behçet's disease were meningo-encephalitis (13 cases), febrile meningeal syndrome (3 cases), intracranial hypertension (6 cases), polyneuritis of the lower limbs (1 case), and isolated retrobulbar ocular neuritis (1 case). Several classical notions concerning the "Neuro-Behçet" meningo-encephalitis were confirmed: the frequency of central motor lesions (33 p. cent), cerebrospinal fluid alterations (anomalies in 100 p. 100 of cases in the initial stage), and the often unfavorable course (40 p. cent). An unusual finding in this series was the frequency of cerebral veins thrombosis (4 certain and 2 probable). These could be differentiated from meningo-encephalitis by their symptomatology, predominantly that of intracranial hypertension, and by their course: often the first disorder to appear in the course of Behçet's disease, they followed a favorable neurological course but were constantly complicated by other vascular manifestations, usually phlebitis. It is suggested that a long-term anticoagulant treatment should be associated with corticoid therapy in these forms.

Morphology of the renal medulla in ischemic acute renal failure in the rat.

In the initial phase of ischemic acute renal failure in the rat the outer medulla is characterized by widening of peritubular capillaries in the inner stripe and by accumulation of cytoplasmic blebs in dilated proximal straight tubules in the outer stripe. Both findings contribute to tubular obstruction. In the maintenance phase, outer and inner stripes show tubular necrosis mainly of proximal straight tubules and thick ascending loops of Henle. In both phases the papilla is apparently spared from damage. Protective measures act at least partly by prevention of peritubular capillary widening in the inner stripe of outer medulla.