Identification and treatment of symptoms associated with inflammation in medically ill patients.

Medically ill patients present with a high prevalence of non-specific comorbid symptoms including pain, sleep disorders, fatigue and cognitive and mood alterations that is a leading cause of disability. However, despite major advances in the understanding of the immune-to-brain communication pathways that underlie the pathophysiology of these symptoms in inflammatory conditions, little has been done to translate this newly acquired knowledge to the clinics and to identify appropriate therapies. In a multidisciplinary effort to address this problem, clinicians and basic scientists with expertise in areas of inflammation, psychiatry, neurosciences and psychoneuroimmunology were brought together in a specialized meeting organized in Bordeaux, France, on May 28-29, 2007.

[Effects of the association of sulbutiamine with an acetylcholinesterase inhibitor in early stage and moderate Alzheimer disease].

The efficacy of the inhibitors of acetylcholinesterase in Alzheimer's Disease (AD) is moderated and some patients do not respond to these treatments. Sulbutiamine potentializes cholinergic and glutamatergic transmissions, mainly in hippocampus and prefrontal cortex. This multicentric, randomized and double-blind trial evaluates the effects of the association of sulbutiamine to an anticholinesterasic drug in cognitive functions in patients with AD at an early stage (episodic memory, working memory, executive functions, attention).

Chronic treatment with sulbutiamine improves memory in an object recognition task and reduces some amnesic effects of dizocilpine in a spatial delayed-non-match-to-sample task.

The effect of a sulbutiamine chronic treatment on memory was studied in rats with a spatial delayed-non-match-to-sample (DNMTS) task in a radial maze and a two trial object recognition task. After completion of training in the DNMTS task, animals were subjected for 9 weeks to daily injections of either saline or sulbutiamine (12.5 or 25 mg/kg).

[Effects of sulbutiamine (Arcalion 200) on psycho-behavioral inhibition in major depressive episodes].

Unlabelled: Psycho-behavioural inhibition is characteristic of major depressive disorder and frequently recedes after the other depressive symptoms. This may induce an important psychosocial impairment which could be a risk factor for relapse.

Methods: The aim of this eight weeks, multicentric, randomized, double blind, placebo controlled trial was to assess the efficacy and safety of sulbutiamine (Arcalion) [600 mg p.

Pain and its treatments.

Among many relevant topics concerning pain and its treatments, the following will be considered: (1) definition of pain; (2) physiopathology; (3) methodology for clinical trials in pain research (4) use of drugs and surgical management of pain, and (5) future directions. The definition of pain as an unpleasant subjective, sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage, does not apply to living people incapable of self-report. Thus, nonverbal behavioral information is often needed and used for pain assessment.

Pharmacology of neuropathic pain.

The development of new animal models now allows the pharmacological study of the neuropathic pain. Our results concern mainly antidepressants and opiates; although the results are incomplete, they show that the different components of the pain syndrome depend on various mechanisms and require adapted treatments and that the treatment must begin as soon as possible, before plastic processes sustain a vicious circle of pain. In the future, pharmacological studies will permit better specification of indications for drugs already used, as well as the associations that improve their efficacy; studies will also encourage development of new treatments more adapted to the physiopathology of the pain syndrome.

[Platelets and migraine].

Platelet function studies in migraine patients have evidenced a number of anomalies (hyperreactivity and serotonin metabolism disorders) that have been suggested as causative factors in migraine attacks. However, a review of the literature shows that these disorders are inconsistent and are probably consequences rather than causes of the headache, although they may contribute to the pathophysiology of the attack. From a broader perspective, the demonstration of platelet dysfunction in migraine raises questions as to the source of these disorders (secondary to plasma factors or due to platelet anomalies) and their significance (do they have any link with transient ischemic attacks or central serotonin neurotransmission dysfunction?).

[Serotonin agonists and antagonists in migraine].

Serotonin agonists (for the acute treatment of attacks) and antagonists (for prophylactic treatment) are the most widely used drugs to treat migraine. However, their effectiveness is not complete and their use is limited by side effects. The activity and presumptive mode of action of these drugs provide support for the role of serotonin in the pathophysiology of migraine and suggest that the trigeminal-vascular system is at the center of the attack; however, other factors and mechanisms may also be involved.

Dopaminergic insufficiency reflecting cerebral ageing: value of a dopaminergic agonist, piribedil.

Amongst the various disturbances of neurotransmission accompanying cerebral ageing, dopaminergic insufficiency is undoubtedly the most constant, the earliest and the most severe. It affects the three ascending dopaminergic systems and may explain many of the motor, emotional, affective and cognitive disorders associated with cerebral ageing. In particular, the psychobehavioural syndrome of cerebral ageing is marked by disorders affecting the capacities for abstraction, conceptualization, reasoning, elaboration of strategies and problem-solving and therefore analogous to those of frontal symptomatology.

[Pharmacological treatment of neuropathic pain].

Neuropathic pain, i.e., pain resulting from functional changes in peripheral and central pathways subsequent to injury to the peripheral nervous system, offers a most difficult challenge to therapy.

Alcohol and central neurotransmission.

The study of the relationships between alcohol consumption and central neurotransmission is difficult: they are different from one individual to another, from one neurotransmission system to another and from one cerebral area to another. Moreover, there is no fully satisfactory animal model of alcoholism and the human studies have to cope with a lot of methodological problems. In spite of these difficulties a bidirectional relationship between alcohol and central neurotransmission is well established.

[Incomplete regressive obstruction of the internal carotid artery in a female patient with fibromuscular dysplasia].

The authors report on the case of a 48-year-old woman, with no history of cardiovascular disease, presenting with a progressive right cerebral deficiency syndrome predominating in the parietal region. X-ray, arteriography and CT scan findings led to the diagnosis of right middle cerebral artery ischemic stroke, in the proximal territory, due to a practically complete occlusion of the right internal carotid artery. The patient recovered and a right carotid arteriography performed 8 months after the initial one showed repermeation of the carotid artery, as well as evidence of fibromuscular dysplasia (FMD).

[Occlusive arteriopathy of the circle of Willis with outlined "Moya-Moya" network in a woman with migraine under oral contraception. Regressive course].

A 19-year-old woman with migraine under contraceptive therapy had transient right hemiparesis due to a minor lesion in the left hemisphere, which was probably hemorrhagic rather than ischemic. On the left side, angiography showed nearly complete obstruction of the terminal portion of the internal carotid artery, extending to the initial portion of its terminal branches, with an outlined "Moya-Moya" network. On the right side, moderate annular stenosis of the cervical portion of the internal carotid was visible.

[Involvement of the peripheral and pyramidal nervous system in Crohn disease. Determining role of folic acid deficiency].

We report on the case of a 16-year-old male patient who presented with a peripheral neuropathy remarkable by the severity of pain, the proximal involvement and the association with an underlying myelopathy. All these symptoms coincided with an acute exacerbation of Crohn disease (regional enteritis) involving mainly the duodenojejunal segment, and were ascribed to a major folic acid deficiency, with total recovery following supplementation. In this connection we recall the various neurological symptoms induced by folic acid deficiency.

[The role of evoked potentials in the diagnosis of multiple sclerosis].

Diagnosis of multiple sclerosis is based mainly upon evidence of inflammation in the cerebrospinal fluid and of diffuse neurological involvement. The second feature is often lacking at onset. It is important to establish the diagnosis as early as possible.

[Chronic hepatic encephalopathies. Acquired cerebral degeneration not due to Wilson's disease].

We report on 4 cases of perennial hepatic encephalopathy and review similar published cases. The neurological picture consists of a cerebellar syndrome, both static and kinetic, dysarthria, choreo-athetoid abnormal movements and mental deterioration. Symptoms are permanent and usually worsen progressively.

[Histological lesions and changes in neurotransmitter systems in the aged brain. Discussion of their pathogenic role].

The histological lesions of cerebral senescence are varied. Some, like congophil angiopathy, are specific to pathological ageing while others, such as neurofibrillary degeneration or senile plaques, are common to all senescence processes. All these lesions reflect disorders in neuron metabolism and synaptic function.

[Parkinson disease and depression (author's transl)].

Depression and Parkinson disease, two very different conditions at first sight, have much more intricate connections than is usually believed. Depression may be the patient's reaction to Parkinson disease, a condition that is anticipated with anxiety, with good reason as it is often very disabling and has not been significantly prolonged by dopamine therapy. Depression may precede the first signs of Parkinson disease.