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We studied 21 consecutive patients from the Lausanne Stroke Registry, who had first-ever ischemic stroke and lone atrial fibrillation, with a standard protocol of investigations including brain CT, and non-invasive cardiac and arterial tests. Rarity of associated risk factors and extracranial; arterial disease, presence of distal intracerebral occlusions on early angiography, and topography of cerebral infarct suggested that cardioembolism was the cause of stroke, though echocardiographic evidence for an atrial thrombus was uncommon. There was no recurrence during a post-stroke 14-day phase, during which anticoagulant and antiaggregant therapies were systematically avoided. Though low, the main risk of stroke recurrence was 0.99 per 100 patient-years during a mean follow-up period of 4.8 years, including a mean duration of anticoagulant therapy of 2.3 years in 18 patients. On the other hand, no death, severe cardiac events, or disabling anticoagulation-related hemorrhages occurred.

During a 5-year period, 85 patients with TIAs, 65 patients with embolic brain ischemia of cardiac source and 50 patients with progressing stroke received intravenous heparin within 96 h. Twelve (6%) developed an early bleeding in the area involved by ischemia. In the 2 cases with transient ischemic attacks (TIAs) (2.3%), major functional sequelae persisted and the 2 cases with emboli from heart (3.2%) died, whereas among the 8 cases with progressing stroke (16%), only 3 worsened from anticoagulant-induced bleeding. Intracerebral bleeding was not associated with excessive anticoagulation or high blood pressure and was related to a large infarction only in the cases with emboli from the heart. Among the 108 patients who were placed on acenocoumarol during 3-12 months after heparin therapy, only one (0.9%) suffered a hemorrhagic infarct from a probable recurrent embolization. The risk of anticoagulant-induced intracerebral bleeding is quite different between the varieties of preceding ischemic events, with different subsequent impact on prognosis.

Autologous fat injection for soft tissue augmentation in the face is claimed to be a safe procedure. However, there are several case reports in the literature where patients have suffered from acute visual loss and cerebral infarction following fat injections into the face. Acute visual loss after injection of various substances into the face is a well-known complication of such interventions. We report two further patients who suffered from ocular and cerebral embolism after fat injections into the face. For the intravasation of fat particles there are three preconditions: well-vascularized tissue, fragmentation of parenchyma, and, especially, a local increase in pressure in the affected tissue. Fat injections into the face lead to an acute local increase in pressure in highly vascularized tissue. We assume that fragments of fatty tissue reach ocular and cerebral arteries by reversed flow through branches of the carotid arteries after they are introduced into facial vessels. The manifestation of fat embolism appears either immediately after the fat injection or after a latency period. Fat embolism can remain subclinical and may not be recognized, or the clinical features may be misinterpreted. To minimize the risk of such a major complication, fat injections should be performed slowly, with the lowest possible force. One should avoid fat injections into pretraumatized soft tissue, for example, after rhytidectomy, because the risk of intravasation of fat particles may be higher. Metabolic disturbances such as hyperlipidemia may also contribute to the clinical manifestation of fat embolism. Routine funduscopic examinations after fat injections into the face could help to provide data for future estimation of the patient's general risk.

We report four patients with various degrees of chronic, tonic, mildly painful, or non-painful, kyphoscolioses in orthostatism, which developed weeks, or months, after one or several laminectomies for lumbar disk hernia, in the absence of recurring radicular pain or acute lumbar pain. No family history or personal antecedent, of focal or generalized dystonia was found and the dystonia was not seen in any of the four patients pre-operatively, or during the immediate post-operative period. Only ill-defined lumbar 'discomfort', unlike their pre-operative lumbago, was reported by the patients, before and during the occurrence of the pathologic trunk posture on standing. Asymmetric lumbar muscle tonic contraction and hypertrophy was found on physical examination. In all patients, the kyphoscoliosis was maximal when standing, partially disappeared when seated, and completely when lying down. One patient responded well to clonazepam, but the other three showed no improvement with either clonazepam or local injections of botulinum toxin; L-dopa was ineffective in all cases, and trihexiphenidyle in three.

We have examined the clinical features of patients with femoral neuropathy and the factors that influence the prognosis. Of 80 consecutive patients referred for neurophysiological evaluations of proximal lower limb weakness, 32 fulfilled strict inclusion criteria and had adequate information, including estimates of axon loss (AxL) by stimulation of the bilateral femoral nerve. In 31, the Kaplan-Meier method was used to describe the time course of the outcome, while logistic regression was employed to determine the contributing factors. Excellent, satisfactory, and poor outcomes were seen in 10 (31%), 11 (34%), and 10 (31%) patients, respectively. Logistic regression analysis of seven factors demonstrated that the estimate of AxL was the only significant variable. The best prognostic factor was an estimate of AxL ≤ 50%, with all patients fulfilling this criterion showing improvement within 1 year; fewer than half the patients with AxL >50% should be expected to improve. This study clearly shows that, irrespective of the cause of femoral neuropathy, functional improvement is seen in 2 out of 3 patients within 2 years and that the estimate of AxL is the only factor influencing prognosis. © 1997 John Wiley & Sons, Inc. Muscle Nerve, 20, 205–211, 1997.

Background: The risk of stroke and the long-term prognosis of recurrent strokes in young patients with patent foramen ovale (PFO) are not well known. For this reason, the treatment of these patients remains empirical. An alternative treatment to prolonged antithrombotic therapy may be surgical closure of the PFO. Methods: Thirty patients (20 men and 10 women) with stroke and PFO were prospectively selected among 138 patients with stroke and PFO for a study of surgical closure of PFO at our center. Eligible patients were 50 microbubbles counted in the left atrium on contrast transesophageal echocardiography (TEE), and (4) Valsalva maneuver or cough preceding the stroke. Patients selected in this manner for surgery were considered to be a subgroup with a higher risk of stroke recurrence. Results: All patients had a direct suture of PFO while under cardiopulmonary bypass without recorded early or delayed significant complication. All patients underwent a new brain MRI and TEE simultaneous with transcranial Doppler ultrasonography after contrast injection at 8 +/- 3 months after surgery. After a mean follow-up of 2 years without antithrombotic treatment, no recurrent cerebrovascular event (stroke or transient ischemic attack [TIA]) and no new lesion on MRI had developed. Postoperative contrast TEE and transcranial Doppler ultrasonography showed that two patients had residual interatrial right-to-left shunting, although much smaller than before surgery, associated with single versus double continuous suture. Conclusions: Our study of 30 selected stroke patients with surgical suture of PFO showed a stroke recurrence rate of 0% and no significant complication. Residual right-to-left shunting may be avoided by double continuous suture of the PFO. In the absence of controlled studies to guide individual therapeutic decisions, our findings show that PFO closure can be done safely and may be considered to avoid recurrence in selected patients with long life expectancy and presumed paradoxic embolism.NEUROLOGY 1996;47: 1162-1166

Using a published protocol, we evaluated a non-selected population of stroke patients to identify unnecessary days of hospitalisation in the Department of Neurology at the Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland. This study was undertaken to determine whether physicians can modify the non-medically justified hospital days. We prospectively studied 118 patients with stroke admitted to our Department over a period of 5 months. Each day spent on the ward was placed in one of two categories: those due to medical reasons (1,391 hospital days) and those due to non-medical reason (518 days). Using a previously published protocol, 74 parameters were evaluated. Delays in obtaining examinations or a specialist's consultation accounted for a small proportion of waiting days (1.9% of total hospital days), which was greater in patients who were not disabled (0.9% of hospital days) than in patients with total dependence (0.2% of hospital days). The delays resulted mainly from awaiting transfer either to another department or to a nursing home. The length of stay increased with severity of dependence. However, the number of days spent for transfer to a nursing home was also relatively high in the non-dependent patient group (42% of hospital days). This study demonstrates that neurologists cannot easily influence the length of stay in hospital. It also corroborates the need to develop short- and long-term chronic care facilities to facilitate the transfer of patients once there are no further medical reasons for staying in hospital.

We report two patients with subacute diffuse encephalopathy characterized by confusion, myoclonic encephalopathy, and mild akineto-rigid extrapyramidal signs in one case and by apathy, memory deficit, and partial complex seizures in the other. Hashimoto's thyroiditis with high titers of anti-thyroglobulin antibodies was diagnosed in both patients, who were unresponsive to anticonvulsant medication, but showed rapid neurological improvement following steroid treatment. On neuropsychological examination, predominant frontotemporal dysfunction was noted. Electroencephalographic activity was remarkable for its rhythmical delta activity, unresponsive to, or even paradoxically increased by, anticonvulsant treatment. On magnetic resonance imaging, atrophy with temporal predominance was found. These observations support the idea that this potentially treatable dementia and movement disorder should be classified as a separate clinical entity.

Neuronal growth factors hold promise for providing therapeutic benefits in various neurological disorders. As a means of ensuring adequate central nervous system delivery of growth factors and minimizing significant adverse side effects associated with systemic delivery methods, we have developed an ex vivo gene therapy approach for protein delivery using encapsulated genetically modified xenogeneic cells. Ciliary neurotrophic factor (CNTF) has been shown in various rodent models to reduce the motor neuron cell death similar to that seen in amyotrophic lateral sclerosis (ALS). The initial trials focusing on the systemic administration of CNTF for ALS have been discontinued as a result of major side effects, thus preventing determination of the potential efficacy of the molecule. In order to deliver CNTF directly to the nervous system, we conducted a phase I study in which six ALS patients were implanted with polymer capsules containing genetically engineered baby hamster kidney cells releasing approximately 0.5 microgram of human CNTF per day in vitro. The CNTF-releasing implants were surgically placed within the lumbar intrathecal space. Nanogram levels of CNTF were measured within the patients' cerebrospinal fluid (CSF) for at least 17 weeks post-transplantation, whereas it was undetectable before implantation. Intrathecal delivery of CNTF was not associated with the limiting side effects observed with systemic delivery. These results demonstrate that neurotrophic factors can be continuously delivered within the CSF of humans by an ex vivo gene therapy approach, opening new avenues for the treatment of neurological diseases.

The gene therapy approach presented in this protocol employs a polymer encapsulated, xenogenic, transfected cell line to release human ciliary neurotrophic factor (hCNTF) for the treatment of Amyotrophic Lateral Sclerosis (ALS). A tethered device, containing around 10(6) genetically modified cells surrounded by a semipermeable membrane, is implanted intrathecally; it provides for slow continuous release of hCNTF at a rate of 0.25 to 1.0 micrograms/24 hours. The semipermeable membrane prevents immunologic rejection of the cells and interposes a physical, virally impermeable barrier between cells and host. Moreover, the device and the cells it contains may be retrieved in the event of side effects. A vector containing the human CNTF gene was transfected into a line of baby hamster kidney cells (BHK) with calcium phosphate using a dihydrofolate reductase-based selection vector with a SV40 promoter and contains a HSV-tk killer gene. hCNTF is a potent neurotrophic factor which may have utility for the treatment of ALS. Systemic delivery of hCNTF in humans has been frustrated by peripheral side effects, the molecule's short half life, and its inability to cross the blood-brain barrier. The gene therapy approach described in this protocol is expected to mitigate such difficulties by local intrathecal delivery of a known quantity of continuously-synthesized hCNTF from a retrievable implant.

We report the cases of two patients presenting a peculiar speech disorder, which we have named "echoing approval", in which the patients echo, in replying to questions in a dialogue with short phrases, the positive or negative syntactical construction of a question, or its positive or negative intonation, but without any repetition of whole or part of sentences. When asked about their symptoms, the patients replied 80% of the time with "yes, yes", "that's right", or "exactly" to positive questions and "no, no" or "absolutely not" to negative questions, regardless of their actual symptoms and oblivious to self-contradiction. In addition, when the examining doctor was speaking to a medical colleague in the patient's presence and using medical terminology that the patient did not understand, he/she agreed or disagreed with any sentence and technical word uttered in a way entirely dependent on the syntax or intonation used. To distinguish this speech disorder from echolalia or verbal perseverations, with which it may be superficially confused, we suggest that it be called "echoing approval", as it may be part one of the manifestations of the environment-dependency syndrome. This clinical picture was found to be associated with features of transcortical motor aphasia and frontal lobe signs. One patient had a bilateral callosofrontal malignant glioma and the other a probable multiple system atrophy with global deterioration, pre-eminent frontal release signs, diffuse leukoencephalopathy and multiple lacunes. On the basis of these clinical deficits and neuroimaging features, we are unable to delineate the common, or minimal, lesioned network required for this symptomatology to occur, especially in the absence of a series of patients, and with such a difference in both the location and causes of the lesions. However, bilateral frontosubcortical dysfunction was pre-eminent in the clinical picture in both patients, even though more diffuse brain pathology was seen in one, and it might be speculated that dysfunction of the bilateral orbitofrontal and frontomesial motor frontosubcortical circuits might be involved in the aetiology of this peculiar speech disorder.

Article abstract-We describe a patient who had sequential strokes in both hemispheres with a severe unilateral spatial neglect after a first right-sided parietal infarct and abrupt disappearance of the neglect after a second left-sided frontal infarct. The first lesion involved the caudalmost right angular gyrus (area 39), whereas the second lesion involved the left frontal eye field (area 8) and surrounding cortex. Those two cortical areas are assumed to have a pivotal role in modulating both shifts of attention within extrapersonal space and saccadic eye movements through their connections with subcortical structures, in particular, superior colliculi and thalamic nuclei. Our case supports the existence of a distributed anatomic-functional network in subserving directed spatial attention.NEUROLOGY 19;: 184-189

We studied 8 patients with stroke and hemineglect, who presented with a transient active orientation and explorative behavior, turning head, eyes, and trunk in the opposite direction to any stimuli given in the neglected hemispace, as if repelled. This peculiar active behavior increased on repetitive stimulation, with the patient turning over by more than 180 degrees, with extreme rotation and opisthotonos-like extension of the axial muscles, as if looking for something behind him, his pillow or his bed. This behavior fluctuated during the day and vanished after a few days. We coined the term "hyperneglect" for this behavior, postulating a higher degree in the neglecting behavior or an additional field of hemineglect in the non neglected hemispace, or the release of repellent active behavior from parietal origin by the acute lesion. On CT, five patients showed two sequential uni- or bilateral hemispheric strokes of different ages on CT, while two patients had a large, unilateral infarct associated with hypertensive leukoencephalopathy and contralateral brain edema respectively. This behavioral syndrome seems to be associated with an acute stroke involving the frontal or parietal lobes and a previous lesion in the same or the opposite hemisphere.

We report a patient with a small infarct in the posterior thalamic nuclei involving the pulvinar, probably in the territory of the lateral branches of the left posterior choroidal artery, who first pr

A 70-year-old right-handed woman developed a complete Klüver-Bucy syndrome including psychic blindness, aberrant sexual behavior, hypermetamorphosis, aphasia and visual agnosia following left anterior temporal lobectomy for an anaplasic oligodendroglioma. MRI showed no argument for a contralateral ischemic infarct, tumoral growth or white matter damage. Thus the possibility that a unilateral anterior temporal lesion can cause the whole picture of Klüver-Bucy syndrome must therefore be considered.

A patient with spontaneous intracranial dissection in the carotid system and fatal outcome is presented. A review of 59 patients reported in the literature shows that this condition has different epid

We report the cases of three patients with a thalamic infarct in the territory of the posterior choroidal artery involving the posterior thalamic nuclei. These patients developed delayed complex hyperkinetic motor syndromes, associating ataxia, tremor, dystonia, myoclonus and chorea, which we call "the jerky dystonic unsteady hand". One patient had a severe myoclonic and ataxic-dystonic choreoathetosis; another showed a so-called rubral tremor (myoclonic ataxia with resting, action, and wing-beating tremor) with dystonia; and the third one had a dystonic and ataxic hand with intermittent mild action myoclonus. All of them had sensory dysfunction; two had also presented with a painful Dejérine-Roussy syndrome. All had CT or MRI-proven infarcts in the territory of the posterior cerebral artery involving the posterior choroidal territory with an abnormal signal in the posterior area of the thalamus (pulvinar nucleus) but sparing the other thalamic, subthalamic and midbrain structures. These delayed myoclonic complex hyperkinetic syndromes have not been reported before, and we did not observe them in other topographic forms of thalamic infarcts. They may thus represent a new entity of movement disorders due to lesions in the posterior thalamic nuclei, with specificity for posterior choroidal artery infarcts.

Atrial fibrillation (AF) is a risk factor for stroke, although it may not always be directly responsible for the stroke. On the other hand, cardiac arrhythmias and electrocardiographic changes have been reported after ischemic stroke and numerous other intracranial pathologies. We tested the hypothesis that some patients with acute stroke may develop transient AF as a consequence of the stroke. This study was based on 1,661 patients with first-ever stroke consecutively hospitalized and prospectively included into the Lausanne Stroke Registry. "Recent AF" was defined as AF discovered at or after ("after-admission" AF) admission in patients without any previous history of AF. Populations with recent AF and after-admission AF were compared for AF evolution, risk factors, and lesion type and distribution with patients with previous history of AF (known AF) and with patients with another recognized cardiac source of embolism (cardioembolic). Twenty-four patients had recent AF on admission, and 17 developed it a few hours to 3 days after stroke. AF disappeared after a few days in 26 (63%; 94% of after-admission AF) patients. Stroke was a primary hematoma in 9.8% of patients with recent AF, 2.8% of patients with known AF, and 0.9% (p < 0.001) of patients with cardiac source of embolism. Parietoinsular (32%) and brain stem (11%) involvement were more common in recent AF than in cardioembolic stroke in general (16.7% and 6.7%, respectively; p < 0.05). AF discovered after an acute stroke lasted no more than a few days, suggesting that it may have occurred as a consequence of the stroke. This possibility is emphasized by the significant predominance in patients with recent AF of primary hematoma, which cannot be caused by AF, and of parietoinsular and brain stem involvement, which are experimentally known as arrhythmogenic. This hypothesis should be considered in patients with acute stroke and previously unknown AF before therapeutic decisions are made.

We assessed the validity of clinical diagnosis of topography (CDT) and etiology (CDE) in 100 consecutive patients who were examined within 12 h of stroke onset by a stroke team (1 neurologist with int

We report a patient with recurrent cardioembolism and hemorrhagic infarcts, who developed a fatal intracerebral hemorrhage 3 days after intravenous anticoagulation. At autopsy, cerebral amyloid angiopathy (CAA) was found. Because CAA and anticoagulation may add up to trigger cerebral hemorrhage, the possibility of underlying CAA should be raised before anticoagulating elderly patients with stroke.

167 of 1,802 patients with first strokes, admitted to a stroke primary care center and included prospectively into the Lausanne Stroke Registry had sensorimotor stroke (SMS) involving face/upper limb/

Intraluminal thrombi in the carotid circulation are uncommonly reported as a cause of stroke in young adults. We report two young women who suffered an embolic cerebral infarction from a floating thrombus in the innominate artery, without clotting abnormalities. Intraluminal thrombus at that level may have been previously overlooked as a cause of embolic cerebral infarction in young patients, because of the lack of a systematic assessment of the aortic arch and its proximal branches. Taking into account the fact that the evolution may be rapidly fatal, this possibility should be considered early in young patients without a clear etiology of stroke.

We studied 12 patients (6 men and 6 women) with a mean age of 47 years with stroke (n = 11) or transient ischemic attack (n = 1) in relation with an atrial septal aneurysm. Ten patients showed also a

Perioral and distal upper limb sensory dysfunction (cheiro-oral syndrome) has classically been attributed to cortical involvement. In previously reported cases of the syndrome, caused by stroke, however, the thalamus or brain stem has been the actual site of the lesion. We have studied two patients with infarct in the superficial middle cerebral artery territory involving the parietal operculum. Sensory involvement was purely subjective in the face, but severe hypoesthesia was present in the distal upper limb, involving mainly position sense, stereognosis, and graphesthesia. Temperature and pain sensation were involved in one patient. These findings correlated with involvement of the lower part of the postcentral gyrus, more caudal parts of the parietal operculum, and underlying white matter. This opercular cheiro-oral syndrome seems more uncommon than faciobrachiocrural hemihypesthesia associated with anterior parietal artery territory infarct. A double supply to the parietal opercular region through branches of the temporal arteries and anterior parietal artery may explain the rarity of cheiro-oral syndrome resulting from hemisphere stroke, because simultaneous and partial compromise to two different pial artery networks is uncommon.

The incidence of anti-GM1 antibodies in the serum of 104 patients with neurological diseases, 35 patients with non-neurological diseases (NND) and 41 normal controls was determined by enzyme-linked immunosorbent assay (ELISA). Anti-GM1 antibodies were found in 90% of patients presenting with a motor neuropathy (all except one had multifocal conduction blocks). A large proportion (60%) of these patients displayed high antibody titer ranging from 101 to 788. A low incidence of anti-GM1 antibodies was found in the other groups of patients, i.e. 21% of amyotrophic lateral sclerosis (ALS), 26% of other neurological diseases (OND) and 23% of NND. High antibody titers ranging from 106 to 260 were found in two (5%) ALS patients, one (2%) OND patient (myasthenia gravis), and one (3%) NND patient (Waldenström's disease). This study shows that high titers of anti-GM1 antibodies are found in a large proportion of patients with motor neuropathy with multifocal conduction blocks. This argues for a possible autoimmune origin of this neuropathy. We suggest that anti-GM1 antibody determination should be included systematically in the evaluation of all patients with motor neuron diseases and predominantly motor neuropathies.

Resume L'alpha-coma associe un coma et des modifications de l'EEG caracterisees par un rythme de base variant entre 8 et 13 Hz, d'une amplitude inferieure a 50 gmV, de repartition diffuse sur tout l'encephale, et depourvu de reactivite aux stimulations sensorielles. Vingt cas d'alpha-coma sont decrits: 16 cas sont en rapport avec une encephalopathie anoxique, deux cas concernent des accidents vasculaires dans le tronc cerebral, et deux cas sont secondaires a une encephalopathie metabolique. Les hypotheses concernant l'origine des modifications de l'EEG dans l'alpha-coma sont revues, bien que les mecanismes etiopathogeniques soient mal compris.

• We studied 13 patients with supranuclear lower cranial nerve ("pseudobulbar" or "suprabulbar") palsy of acute onset. While seven patients had had a prior stroke, six patients had no history of stroke. Eight patients experienced a complete bilateral supranuclear lower cranial nerve palsy, which was isolated in five patients and associated with hemiplegia and with hemiparesis in three patients. Pseudobulbar palsy was partial in five patients. Only one patient had neuropsychologic impairment. The pseudobulbar features improved or recovered within a few weeks in all patients. The common characteristic of the lesions on computed tomography or magnetic resonance imaging was the interruption of the corticonuclear pathways contrasting with marked sparing of the corticospinal pathways in both hemispheres. These lesions were either an opercular infarct, or a deep infarct in the corona radiata or internal capsule, or a lenticular hemorrhage. Hypertension was the most prevalent concomitant. Our findings suggest that acute pseudobulbar or suprabulbar palsy has rather stereotyped anatomic-vascular correlates and time course.

Two patients with bilateral thalamo-mesencephalic infarct in the paramedian territory developed vertical gaze dysfunction and marked behavioural changes, in the absence of significant motor inability and formal neuropsychological impairment. While they were physically and emotionally active before stroke, they became apathetic, aspontaneous, indifferent, and seemed to have lost motor and affectic drive, as well as the need itself for any psychic activity. However, this mental and motor inertia was reversible when the patients were repeatedly stimulated by another person. This need for constant external programming, together with a lack of emotional reactivity, made the patients resemble robots. CT and MRI suggested involvement of the dorsomedial and midline nuclei of the thalamus, and SPECT showed remote frontomesial hypoperfusion. A disturbance of the striatal-ventral pallidal-thalamic-frontomesial limbic loop is suggested by previous reports of a similar "loss of psychic self-activation", "pure psychic akinesia", or "athymhormia" with bipallidal, bistriatal, or subcortical bifrontal lesions.

In a 67-year-old man with left horizontal homonymous sectoranopia and slight facio-brachial hemiparesis, CT showed recent infarction in the right posterior choroidal-artery region. This particular vis

Small ''lacunar'' infarcts in the territory of the deep perforators (ITDP) have usually been attributed to small-vessel disease associated with hypertension or diabetes, but recently also to embolism

We report clinicotopographic correlations in 2 patients with central hypoventilation and unilateral infarct in the caudal brainstem. One patient had nearly complete loss of ventilation involving both automatic and voluntary components. He showed no ventilator response during a CO2 retention test (PaCO2 62 mm Hg, PaO2 82 mm Hg), while consciousness was preserved until death. The infarct involved the reticular formation, nucleus tractus solitarius, nucleus ambiguus, and nucleus retroambiguus on the right but spared the dorsal motor nucleus of the tenth cranial nerve, and sensory and corticospinal tracts. The second patient showed hypoventilation more selectively involving automatic responses (Ondine's curse). The infarct involved the medullary reticular formation and nucleus ambiguus but spared the nucleus tractus solitarius. We suggest that unilateral involvement of pontomedullary reticular formation and nucleus ambiguus is sufficient for generating loss of automatic respiration, while associated lesion of the nucleus tractus solitarius may lead to more severe respiratory failure involving both automatic and voluntary responses.

We evaluated the association between alcohol consumption and carotid atherosclerosis in 261 consecutive patients greater than 50 years old admitted to our community-based primary-care center with first ischemic stroke; their characteristics were entered into a computerized data bank (Lausanne Stroke Registry). Reported regular alcohol consumption was compared with the presence and severity of internal carotid artery disease as assessed by duplex scanning with spectral analysis of the Doppler signal and real-time B-mode imaging at the level of the carotid bifurcation. We found an inverse linear relation between light-to-moderate alcohol intake (less than or equal to 4 standard drinks/day) and severity of internal carotid artery stenosis. No conclusion could be drawn for heavier drinkers because there were too few. A logistic regression model showed that hypertension, cigarette smoking, and age in men and diabetes mellitus and cigarette smoking in women strongly counterbalanced the potential benefit of alcohol consumption. Although regular alcohol drinking cannot be advocated on the basis of our findings, light-to-moderate consumption of alcohol is the first factor to be inversely associated with extracranial carotid atherosclerosis in symptomatic patients with cerebrovascular disease.

We evaluated the effect of nimodipine (30 mg q.i.d. orally for 14 days) on acute ischemic stroke of mild or moderate severity in a unicenter, double-blind, randomized, placebo-controlled pilot study. Treatment had to be started after CT, within 48 h of infarct in patients with a Mathew scale sum score between 50 and 75. The duration of follow-up was 4 months. Eight of the 60 randomized patients were excluded because of incorrect diagnosis. For the remaining 52 patients, 24 were allocated to nimodipine and 28 to placebo. Analysis of variance and covariance and repeated measurements of the Mathew scale scores showed no difference between the two groups, who had continuous and parallel improvement. There was no recurrent stroke, but 1 control died 4 weeks after stroke. Treatment with nimodipine was well tolerated (hypotension: 1 treated patient, 3 controls; bradycardia: 1 treated patient, 2 controls; sGPT increase: 1 treated patient, 1 control). The lack of efficacy of nimodipine in this study may be due to: (1) the neurologic deficit not being severe enough, or (2) the delay before treatment was too long.

Many patients suffer a stroke early after a transient ischemic attack, but the reason why is often unclear. We studied 12 patients with less than 75% stenosis of the internal carotid artery and a single hemispheric transient ischemic attack lasting less than 1 hour who had a normal neurologic examination 3-13 hours later and a normal computed tomogram 24-36 hours later. Single-photon emission computed tomography using technetium-99m HM-PAO less than or equal to 50 hours after the attack showed no abnormality in eight patients, but in the other four there was an area with 30-50% reduction in perfusion ipsilateral to the transient ischemic attack. Three of these four patients developed an ipsilateral infarct 3-7 days later, but none of the eight patients with normal single-photon emission computed tomograms had a stroke during the following weeks. No difference in therapy, risk factors, severity of internal carotid artery disease, or timing of the technetium-99m study could explain these findings. We suggest that some transient ischemic attacks, though clinically identical to others, may be associated with persisting focal hypoperfusion, which predisposes to early stroke.

The onset of a migraine attack is associated with the activation of the trigemino-vascular system. Early intervention with triptans, which inhibit this activation is an effective treatment for migraine attacks. To avoid a cutaneous allodynia it is necessary to introduce as soon as possible the treatment with triptans. Drugs useful in the migraine prophylaxis tend to reduce the neuronal excitability in different areas of the central nervous system. The new definition of a chronic migraine is presented. This chronic migraine is frequently the result of an overuse of triptans. The practical aspects of the therapy of this specific migraine are described.

The Whiplash Associated Disorders (WAD) are mostly chronic cervical and cephalic pain syndromes. They are often associated with general disorders and with sensorial difficulties. The neurologist evaluates this trouble according to neurochemical and neurophysiological models, hypothesizing a "central hypersensitivity" after a localised peripheral lesion (such as cervical distortion). Other epistemological points of view are certainly legitimate, for example "biopsychosocial" models. From a therapeutic point of view, it seems worth while to try to prevent the development of WAD. When chronic pain is accompanied by difficult life situation, the solution is not simply medical but also social. Faced with a persistent WAD, the therapeutic attitude should be individualised and multidisciplinary, seeking the autonomy of the patient.

Facial pain can represent an expression of an initial symptom of a severe primary neurological disease. Some examples are presented. In the second part chronic pain like facial pain, stomatodynia, odontalgia and temporomandibular disorders are illustrated and grouped together under the name idiopathic facial or orofacial pain. The similar clinical aspects of these facial pains are presented. The concept of nonnociceptive pain and other mecanisms to explain these chronic painful disorders are briefly discussed. Drug treatment like antidepressant and cognitive behavioural therapies are counselling as effective therapies of these chronic pains.

A patient with idiopathic inflammation of the right orbit, established by biopsy, developed episodes of transient left sensorimotor hemiparesis. Neuroimaging showed intracranial extension of the disease with pronounced narrowing of the right internal carotid artery in its intracavernous portion. Oral cyclophosphamide induced gradual improvement. Transient ischaemic attack is rarely found in association with orbital disease and indicates possible intracranial extension.

Elaborate visual hallucinations limited to a hemifield are exceedingly rare. We report a patient with a right striatocapsular infarct who developed formed complex visual hallucinations restricted to t