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Copyright of EMC-Neurologie is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of EMC-Neurologie is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Introduction: Fatigue is a complex, subjective experience, frequent in multiple sclerosis (MS) and stroke patients. The tiredness these patients experience can take on many features depending not only on the cerebral location of the lesions and mood aspects, but also on the pathophysiology of the disease. Thus, it is reasonable to expect that fatigue may have different implications in MS and stroke. The aim of the present work was to compare fatigue syndrome in these two populations. Patients were matched for handicap., Materials and Methods: Seventy-nine stroke and 39 MS outpatients were included with the following inclusion criteria: i) patients with possible or relapsing-remitting MS with an Expanded Disability Status Scale (EDSS) score<2.5, disease duration<6 years, and stable medical condition for at least 6 weeks; ii) stroke patients with mild neurological impairment, i.e. scoring<3 at the National Institute of Health Stroke Scale (NIHSS) one year after stroke; iii) absence of functional impairment (Barthel index=100) and similar negligible handicap (Rankin scale<2 for both groups); no or mild cognitive deficit; iv) neither DSMIV criteria of depression, nor significant anxious/depressive symptoms (Hospital Anxiety and Depression scale; HAD; score<8) in both groups. The Fatigue Assessing Instrument (FAI) was used to assess fatigue., Results: Twenty-nine percent of stroke and 46 p. cent of MS patients had a significant score on the FAI (p<0.05). Multiple regression analysis using groups, gender and age as factors showed a group effect in 3 out of 4 subscales: MS patients scored higher than stroke patients mainly for psychic impact (4.86 vs. 3.28), but also for severity (mean 3.86 vs. 2.97) and specificity (4.36 vs. 3.32). Response to rest (5.36 vs. 6.06) only tended to be better in the stroke group. In the subpopulation with significant fatigue scores, psychic impact was more elevated in the MS group. The functional consequence of fatigue in physical, professional and social activities were similar., Discussion: Fatigue was more severe in MS than stroke patients, independently of disability. The most significant factor in the MS group was the psychic impact, reflecting impaired motivation, concentration and irritability, despite the absence of depression. However, subjective consequences of fatigue on work, family and leisure activities were comparable in both groups.

Neurodegenerative and cerebrovascular diseases have been related for more than a century. Epidemiological data show that main vascular risk factors are also risk factors for Alzheimer disease. Experimental evidences demonstrate that some of those risk factors accelerate the progress of Alzheimer lesions, mainly by acting on the amyloid cascade. Recent advances in understanding the basic mechanisms of CADASIL and familial amyloid angiopathy reveal that these forms of vascular dementias are degenerative disease of brain vessels. Modern neuroimaging techniques will allow to better understand relations between symptomatic strokes, silent infarcts, leukoaraiosis, microbleeds and degenerative pathology before the stage of dementia.

We report on the therapeutic advances in Neurology that took place over the last year. The purpose here is not to provide a detailed and exhaustive listing of each study of 2005, but rather to emphasize those that might be the most significant for the clinician. Following this idea, we have chosen to mention not only the therapeutical advances, but also, sometimes, the disappointments of 2005.

The psychopathology of stroke encompasses several psychiatric and behavioral disorders that have high prevalence in the geriatric population, reduce the patient autonomy and increase the caregiver's burden. These disorders are usually associated with other cognitive and neurological deficits, and are labelled as neuropsychiatric when the whole clinical picture is consistent with the specific dysfunction of a neural system or brain region. Thus the neuropsychiatry of stroke comprises disorders of the perception/identification of the self and the environment (anosognosia of hemiplegia, misidentification syndromes, confabulations, visual hallucinations, delirium and acute confusional state), amotivational syndromes (apathy and athymhormia), disorders of emotional reactivity (blunted affect, emotional incontinence, irritability, catastrophic reactions), poor impulse or ideation control (mania) and personality changes. The clinical profile of the subcortical vascular dementia also points to specific brain dysfunction (frontal-subcortical pathways) that manifests with behavioral (depression, emotionalism, irritability) and cognitive symptoms (psychomotor retardation, attention, executive and memory deficits). However, post-stroke depression and anxiety, which have a more variable clinical presentation and might be assimilated, for several aspects, to post-traumatic or adaptive disorders, are disorders less characterized in their neural correlates.

The aim of this review is to discuss the different treatment strategies of acute stroke. The main studies performed with intravenous or intra-arterial thrombolysis are reported as well as the recent results concerning the use of IIb/IIIa platelet receptors antagonists. We will also discuss the potential effect of ultrasound on systemic thrombolysis. Finally are mentioned the most important measures to avoid medical and neurological complications which may occur during the acute phase of stroke.

Ischemic stroke is an important cause of mortality and invalidity. Focal cerebral ischemia induces multiple and complex mechanisms leading to the loss of function and the demise of cerebral tissue. Apoptosis, or programmed cell death, well known for its role in normal development, is one of these mechanisms, and contributes to ischemic neuronal death. This short review gives an overview of apoptotic mechanisms triggered by cerebral ischemia.

Introduction: Pain may be a presenting symptom of Parkinson's disease or may occur during the motor fluctuation stages of the disease. The complexity and pathophysiology of pain in Parkinson's disease still remains poorly understood., Objective: To characterize clinically the different painful presentations of Parkinson's disease, their relationship to the stage of the disease and their connections with motor fluctuations and treatment., Methods: We reviewed painful syndromes in 388 consecutive parkinsonian patients of the Lausanne Movement Disorders Registry, based on an itemized questionnaire used prospectively to characterize the pain by its description, topography, date of appearance and possible relationship with motor fluctuations. Among these patients with clinically-diagnosed dopa-responsive Parkinson's disease, 269, i.e. 67 percent presented sensory or painful syndromes. Among them, 94 percent had muscular pain: stiffness (85 percent), cramps, pseudo-cramps, spasms (3 percent) or various myalgias (7 percent); 51 percent presented osteo-ligamentar "rheumatologic" pain, articular (23 percent), periarticular (3 percent) or spinal (31 percent), but less defined and localized neurogenic painful syndromes were less frequent (8 percent), such as paresthesia (6 percent), dysesthesia (<1 percent), burning sensation (2 percent), itching (<1 percent), ill defined discomfort (6 percent) or a feeling of heaviness (1 percent), with segmental (86 percent), axial (54 percent), radicular or pseudo-radicular (14 percent), acral distal (4 percent) or less frequently anorectal or visceral distribution. Restless legs or akathisia were occasional (10 percent). Headaches and facial pain were less frequent (1 percent), we did not encounter phantom pain. More than one quarter were present at the beginning of the disease, only (3 percent) of them resolved during the development of the disease. About one-third were clearly linked with motor fluctuations, the majority occurring in off phase (34 percent). We did not find any correlation with age, gender, duration or stage of disease, L dopa equivalent dose, depression, insomnia or autonomic dysfunction., Conclusion: Painful syndromes are found in two thirds of patients with Parkinson's disease, with mainly pain of muscular origin, followed by osteoarticular and neurogenic painful syndromes, a quarter of the patients experience pain in early phases of the disease and a third in relation with motor fluctuations.

Blood pressure is abnormally elevated in acute stroke in most patients. This blood pressure increase is usually transient and associated with a poor prognosis. Lowering blood pressure too importantly during this period may worsen the outcome of the patient. Antihypertensive therapy is therefore required only when blood pressure is severely increased, especially in the presence of intracerebral haemorrhage. Initiating treatment before admission to the hospital is not recommended. The medications to be preferred are the blockers of the renin-angiotensin system, the beta-blocker labetalol (which possesses also alpha-blocking properties) and NO donors.

In this paper, we present the last studies with impact on daily practice and up-to-date guidelines which can lead to a rational approach of the patient with neurological disease. In cerebrovascular diseases, several strategies are discussed to increase the number of patients who can benefit from thrombolysis, whereas in secondary prevention, the association of clopidogrel and aspirin versus clopidogrel has not shown to be beneficial. In Parkinson's disease, the inclusion criteria and benefits of deep brain stimulation are more precisely known. New genetic targets have been found in the field of myopathies, which open new therapeutic perspectives.

Introduction: Hematological diseases are seldom found as the etiology of ischemic strokes, but are frequently investigated by expensive laboratory tests after a first cerebral vascular event., Methods: In the Lausanne Stroke Registry, we retrospectively reviewed the cases of patients hospitalized between 1979 and 2001 for a first ischemic arterial stroke which was attributed to a hematological etiology. Of 4697 patients, 22 (0.47 per cent) had a stroke due to one of the following hematological pathology: polycythemia vera (4), secondary polycythemia (4), essential thrombocytemia (2), secondary thrombocytosis (4), multiple myeloma (1), CIVD (1), protein S deficiency (1), antiphospholipid antibody syndrome (4), moderate homocysteinemia (1). A literature review was undertaken for each hemopathy., Conclusion: In light of the results of these data, we concluded that a complete blood count provides sufficient hematological screening for the majority of patients hospitalized for an arterial stroke. The antiphospholipid antibody syndrome is a rare cause of cerebral infarction, which needs to be investigated in young patients, in cases of multiple or recurring stroke or in the presence of a typical history. Inherited thrombophilias are not a significant risk factor for arterial cerebral infarction and their investigation is only warranted for a sub-group of young patients with a cryptogenic stroke, in which group the prevalence is slightly increased. Moderate homocysteinemia must be considered as a cerebrovascular risk factor of minor importance, but potentially treatable by a substitution of vitamin B12, B6 and folates. The efficacy of this substitution in the prevention of cardiovascular events needs yet to be demonstrated.

The nature and the neurological consequences of the shell wound to the head of the famous French poet Guillaume Apollinaire, on March 17, 1916, during World War I, remain unclear. However, his contemporaries and biographers have been unanimous to state that this event was a major shift in his life. His personality and behavior changed dramatically, and his affective relationships were deeply modified, the most significant example being his rapid disinterest for his fiancée Madeleine, to whom he had written passionate letters nearly every day before the trauma. The study of Apollinaire's letters, scarce medical reports, available memories from friends, and Apollinaire's helmet allow to understand better what brain lesion he had and why neurobehavioral dysfunction developed. While an "intracranial abscess" had been emphasized initially, clinical manifestations, free interval, no infectious problem, and quick resolution of hemiparesis and seizures after a burr hole was performed strongly suggest a chronic subdural hematoma in the right temporal region. Irritability, susceptibility, emotional intolerance, affect flattening, anxiety, and personality change fit perfectly with right temporal lobe dysfunction involving the lateral-basal area. Sparing of mesial-temporal, parietal, and frontal regions explained the absence of significant memory, cognitive, and executive impairment, without disturbed creative skills as a poet and art writer. This cognitive-affective dissociation secondary to isolated right temporal post-traumatic lesion allows to delineate the "deep sorrow" of Apollinaire during the two and a half years before he died from Spanish influenza in 1918.

A painful worsening of known difficulties in walking led us to investigate a man who presented a spastic paraparesis. Radiological investigations had to be repeated three times before making a diagnosis of a right C6 spinal dural arteriovenous fistula after a 22-month follow-up. Knowing the mechanisms leading to spinal venous hypertension may explain the low yield of the early radiological investigations that should be repeated. The efficiency of the treatment depends on the severity of the presurgical neurologic manifestations.

Functional outcome after stroke with severe disability (Barthel Index<60 points) was analyzed retrospectively in one hundred patients, including seventy-three with nonhemorrhagic stroke and twenty-seven with hemorrhagic stroke admitted to our neurorehabilitation center between 1986 and 2000. Neurological deficits and functional disabilities were assessed with the Barthel Index at admission to rehabilitation and after the rehabilitation program in survivors. The rehabilitation therapy was based on the Bobath concept. Patients were not discharged until neurological and functional stability had been reached. There was no difference for age, length of stay, Barthel Index scores at admission and discharged between the groups. Gain in the Barthel Index scores between admission and discharge (p=0.005) resulted from more efficiency in the group with hemorrhagic stroke. These patients appeared to exhibit better functional gain at discharge from rehabilitation than nonhemorrhagic patients. This observation points out that long-term outcome is also better for patients who experience hemorrhagic stroke.

We studied the neurological comorbidity of parkinsonism in 368 consecutive patients from the Lausanne Movement Disorders Registry. Only 6 patients had no neurological comorbidity. We found that 23p.100 of our patients had ischemic strokes, especially large vessel strokes, i.e three times more than in an age-matched control study performed in a recent survey in our country, which is a new finding in contradiction with previous reports mentioning that Parkinson's disease may be a protective factor against stroke. This finding opens new directions for further studies concerning some shared mechanisms in both diseases associated with age. Predominantly tremulous parkinsonism (46p.100) and progressive supranuclear palsy patients (PSP) (40p.100) had the highest prevalence of cerebrovascular disease of all subgroups of parkinsonism, especially lacunar infarcts, which is in accord with a higher frequency of hypertension in these subgroups according to a recent study of ours. Transient ischemic attacks or hemorrhages were not more frequent than in the general population. We did not find a higher frequency of head trauma except for Parkinson's disease, but a trend for a higher frequency of headache and migraine. Brain tumors were more frequent in Parkinson's disease and hydrocephalus and radiculopathies in parkinsonism in general when compared to age-matched populations from the literature. Polyneuropathies were more frequently observed in familial parkinsonism only, but myopathies and cranial neuropathies were not more frequent in our patients. Epilepsy was significantly less frequent in parkinsonism, especially in Parkinson's disease, infectious diseases of the nervous system were rarely encountered, and restless legs syndrome was surprisingly not more frequent than in a normal population. Dementia was associated in 20p.100, but multiple sclerosis is noticeably absent.

The percentage and cause of neuromuscular (NM) diseases have been analysed during a 15-year period of time. A NM disorder was found in 10,852 patients (or 14.4% of all neurological patients seen in our hospital). Mononeuropathies have been the most common causes, followed by polyneuropathies and radiculopathies, but with a variable percentage during time for the most frequent causes, that were carpal tunnel syndrome and diabetic polyneuropathies. Myopathies, diseases of the neuromuscular junction and anterior horn cell disorders counted for 5% among all NM disorders during the first 10 years (1% of all neurological patients) and for 12% during the last 5 years (2.4% of all neurological patients), this period corresponds to the opening of our outpatient clinic dedicated to NM diseases. Among polyneuropathies, the most common causes were diabetes mellitus, chronic inflammatory demyelinating polyneuropathies and the inherited forms of peripheral neuropathies. Among myopathies, the most frequently reported symptom was exercise-induced myalgia. The 2 most common muscular dystrophies (MD) were Steinert myotonic MD, and facio-scapulo-humeral MD. Other myopathies were rare, but of diverse causes, all of them corresponding to the newly introduced definition of Rare or Orphan Diseases.

Atherosclerosis is the most common cause of vascular diseases, but the relevance of cholesterol has only been definitely associated with coronary artery disease and peripheral vascular disease. In comparison, the role of cholesterol in stroke is, while a tempting assumption, subject to controversy in the literature. The crucial question--is cholesterol a risk factor for stroke?--remains open. Recent trials with statin drugs, such as 4 S, CARE, LIPID and WOSCOP, have created a new wave of enthusiasm by showing decreased risk of stroke in the statin-treated patients. However, these trials are most often designed for patients with a known history of coronary artery disease. In contrast, studies investigating the impact of statins in the secondary prevention of stroke are still lacking. Moreover, the beneficial effects of statins on clinical events may involve non-cholesterol mechanisms. In regard to stroke prevention, there is no absolute evidence to recommend the use of statin drug therapy.

Two patients affected with a multiple sclerosis developed cerebral venous thrombosis after lumbar puncture and treatment with intravenous methylprednisolone. In one case, the course was favorable. The second patient died in spite of intracerebral thrombolysis. The autopsy confirmed the diagnosis of cerebral venous thrombosis and multiple sclerosis. We discuss the relationship between lumbar puncture, steroid treatment and cerebral venous thrombosis.

We report the behavioral symptoms presented by a 57-year-old man as the first sign of a Marchiafava-Bignami syndrome and by a 44-year-old woman with centro and extrapontine myelinolysis. These observations define a clinical entity, that we named callosal dementia characterized by: 5) fronto-limbic signs with coarse interjections, repetitive and antisocial behavior, alternation of lack of incitation and agitation; 6) elements of a Balint syndrome (suggestive of a posterior callosal involvement), with a pseudo-hallucinated look and a gaze apraxia; 7) signs of callosal dysconnection and; signs of adjacent white matter involvement, with paucity of vocal and facial expression modulation. Early recognition of these features of callosal dementia may be very helpful for diagnosis of suspected myelinolysis, leading to a more careful research of clinical signs of callosal dysconnection and prompting neuroimaging with MRI. A rapid confirmation of the diagnosis may prevent progression to centro or extrapontine myelinolysis, that may sometimes still be lethal, by adequate supportive measures (slow correction of electrolytes imbalance, correction of deficiencies, total alcohol withdrawal).

We report a case of myositis presenting as an apparently unique progressive facial weakness. The only biological abnormality after an 8-year follow-up was an immunocytoma. Molecular analyses excluded facioscapulohumeral muscular dystrophy. Based on this single case and a review of the literature, we suggest a continuum between focal myositis and generalized myositis.