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There is ample evidence from randomized trials that for patients with stroke, stroke unit care is superior to care in general medical or neurological wards. This evidence, which has been adopted by international guidelines has to be implemented into daily stroke care. This consensus document prepared by the Belgian Stroke Council provides a set of minimum criteria to meet international standards for stroke care. It is intended to provide help in the creation of stroke units in centers who do not currently have one and to provide a benchmark for centres already having organised stroke care.

We report a case of a 51-year-old man presenting with rapidly progressive unilateral tinnitus, hearing loss and imbalance. Neuroimaging revealed bilateral VIIIth cranial nerve masses and multiple cerebral and spinal cord lesions that were interpreted as being acoustic schwannomas and multiple meningeomas. An initial tentative diagnosis of neurofibromatosis type 2 (NF2) was made. Both clinical and radiological evolution were atypical for NF2 and the initial diagnosis of NF2 was questioned. Additional technical investigations demonstrated a pulmonary adenocarcinoma. Postmortem examination confirmed that this patient had multiple central nervous system metastases of a primary pulmonary adenocarcinoma, presenting clinically and neuroradiologically as a probable neurofibromatosis type 2. Clinicians should be aware of the rare possibility of central nervous system metastases mimicking NF2.

Between June 1995 and November 1998, 228 patients with relapsing-remitting Multiple Sclerosis started treatment with glatiramer acetate (Copaxone) 20 mg once daily in the frame of a "compassionate use" protocol in 15 Belgian centers. Following an average treatment period of 5.8 years, treating neurologists were requested to fill in follow-up forms indicating neurological disability status and side effects during the previous 6 months. These data were available for 134 patients. In this group, the Expanded Disability Status Scale (EDSS) improved in 26.3% of patients. An additional 36.8% of patients remained neurologically stable. The Ambulation Index (AI) showed similar results: 12.5% of patients improved, 50% of patients remained stable, and 37.5% worsened. Only 10% of patients dropped out due to several reasons. The adverse events occurring in the period preceding the follow-up survey were non-serious and consistent with the current product information of glatiramer acetate. Among the 94 patients no longer followed-up in the compassionate program, reasons for lost to follow-up were obtained for 63; most of them (41) had stopped GA treatment or switched to another disease-modifying treatment. Overall these results are very similar to the ones reported in the extension study of the pivotal trial (Johnson et al., 2000), and indicate that patients treated with glatiramer acetate have a better outcome than expected on the basis of the natural course of the disease. Despite limitations of the study design, this report confirms the sustained efficacy of glatiramer acetate in reducing the disease progression in patients with relapsing-remitting multiple sclerosis treated in day-to-day clinical practice.

The functional role of the cerebellum is traditionally defined as a mere coordinator of automatic and somatic motor functions. This view determined most of the clinical and experimental investigations of the functions of the cerebellum and overshadowed many attempts to expand its role to non-motor functions. However, during the past decades the collaboration across contemporary neuroscience disciplines has brought about a substantial modification of traditional thinking about the cerebellum. Converging evidence from different neuroscientific angles established the view that the human cerebellum participates in a much wider range of functions than conventionally accepted. Studies have brought to the fore that the cerebellum also modulates neurocognitive functions of at least these parts of the brain to which it is reciprocally connected. In less than two decades, the concept of 'cerebellar neurocognition' evolved from a mere afterthought to an exciting new multifaced area of contemporary neuroscientific investigations. Within this area, one of the major avenues of current research is the role of the cerebellum in non-motor language processing. This paper reviews the recently acknowledged role of the cerebellum in neurocognition and linguistic processes.

This work reviews the current knowledge on epileptogenesis and pathophysiology of epilepsy. Recently, gene defects underlying four monogenic epilepsies (generalized epilepsy with febrile seizures, autosomal dominant nocturnal frontal lobe epilepsy, benign familial neonatal convulsions and episodic ataxia type 1 with partial seizures) have been identified, shedding new light on the pathophysiology of epilepsy as these diseases are caused by ion channel mutations. Although epileptic syndromes differ pathophysiologically, common ictogenesis-related characteristics as increased neuronal excitability and synchronicity are shared as well as mechanisms involved in interictal-ictal transition. Emerging insights point to alterations of synaptic functions and intrinsic properties of neurons as common mechanisms underlying hyperexcitability. This work also reviews the neurochemical mechanisms of epilepsy. An imbalance between glutamate and gamma-aminobutyric acid neurotransmitter systems can lead to hyperexcitability but catecholaminergic neurotransmitter systems and opioid peptides were shown to play a role in epileptogenesis as well. An overview of currently available anti-epileptic drugs and their presumed mechanisms of action is given as an illustration of the neurochemistry of epileptogenesis. Most anti-epileptic drugs exert their anti-epileptic properties through only a few neurochemical mechanisms that are meanwhile basic pathophysiological mechanisms thought to cause seizures.

Animal models are important in the study of the development and expression of focal seizures as well as in the preclinical evaluation of antiepileptic treatment. Many different models are available, including acute and chronic models for simple partial seizures and models for complex partial seizures. Work on models has revealed that the pathophysiology of seizure disorders includes several neurotransmitter and membrane channel alterations. In addition, epileptogenesis of focal epilepsy has been shown to involve the selective loss of neurons and axonal reorganization. Antiepileptic treatment still hinges on three general themes: modulation of voltage-dependent ion channels involved in spike propagation and burst generation, enhancement of GABA-mediated inhibition, and suppression of excitatory amino acidergic activity. Many antiepileptic drugs have proven efficacy against focal seizures in animal models as well as patients. More recently developed antiepileptic drugs may prove to be superior in the alleviation of intractable partial seizures. The three general themes of antiepileptic drug action still dominate the development of antiepileptic treatment strategies. Too much emphasis on the classical models of focal epilepsy may hamper the development of innovative strategies. On the other hand, continued research on new and existing models may broaden our knowledge of the pathophysiological processes underlying focal epilepsy, and inspire new avenues in antiepileptic treatment development.

Primary lymphoma of the central nervous system, until recently representing about 1% of all brain tumours, shows a dramatically increased incidence in the general population as well as in high-risk groups (immunocompromised, AIDS), and may rise up to 6% in a population of AIDS patients. The clinical presentation is variable and cannot reliably be distinguished from other intracerebral tumours. At present, CT and MRI are the methods of choice for diagnosing cerebral lymphomas. However, their characteristics are not specific. The radiological picture may suggest glioma, meningioma, metastatic carcinoma or even a cerebrovascular accident. A labelled somatostatin analogue (pentetreotide) has been proposed as a new tracer for the imaging of somatostatin receptors, which have been identified by immunocytochemical or radioimmunoassay techniques in several organ systems. Somatostatin receptors were also identified in surgical biopsy samples from patients with Hodgkin and non-Hodgkin lymphoma and extracerebral lymphoma has already been visualised in vivo by means of In-111-labelled pentetreotide. While CT images of the brain showed a regression of the tumour after radiotherapeutic treatment, the scintigraphic images showed persistence of the tumoural tissue, corresponding with the clinical evolution and outcome. Furthermore, the absence of extra-cerebral lymphoma tissue, seen on the whole body images, was confirmed by post-mortem examination. To our knowledge, this is the first report of a primary intracerebral lymphoma visualised by means In-111-pentetreotide.

This case report describes an 85 year-old woman who underwent a bilateral frontal lobotomy for presumed schizophrenia 50 years ago. The patient presented with sudden alterations of consciousness accompanied by motionless staring and speech and movement arrest. After 5 to 10 seconds, contact recovered briskly. As there was electrophysiological evidence for a frontal epileptic focus, these fits were classified as complex partial frontal lobe seizures with impairment of consciousness at onset. An aetiological link with the bifrontal lobotomy is probable. At the occasion of this case report, complications of frontal lobotomy are reviewed.

The presented case concerns a 77-year old man who had been chronically taking colchicine for treatment of gout. He was admitted because of a transient ischemic cerebrovascular attack with motor aphasia and complained of preexisting paraesthesias in the lower extremities. Neurological examination revealed a global muscular weakness, absent myotatic reflexes and a diminished sensation. Serum creatine kinase (CK) levels were increased and electromyography showed spontaneous fibrillations in deltoid muscles, positive spikewaves in deltoids and anterior tibial muscles. Motor and sensory conduction velocities were mildly reduced. Nerve biopsy findings were compatible with a chronic axonal neuropathy having produced a significant loss of myelinated axons and also denervation features of unmyelinated axons. In muscle, combined neurogenic and myogenic features were found. The former result from the axonal neuropathy. The latter were mainly characterized by focal myofibrillar disorganisation and accumulation of autophagic vacuoles in muscle fibres. The presented neuromuscular symptoms and signs, the increased CK values, the electromyographic and nerve conduction velocity findings as well as nerve and muscle biopsy observations, are consistent with the diagnosis of colchicine-induced myopathy and neuropathy. Furthermore, the disappearance of paraesthesias, normalisation of CK values, and disappearance of fibrillations and positive spike waves in deltoid and anterior tibial muscles on electromyography, after stopping of the colchicine therapy, supported the diagnosis.

It is now well recognized that poor quality of sleep, with fragmentation as the main characteristic, is a common problem in patients with Parkinson's disease. The effect of a sustained-release levodopa compound (Prolopa HBS) was assessed in a long-term (12 months) study of 15 patients presenting with distressing night time symptoms prolopa HBS was administered only ante noctem, without changing the usual daytime treatment. It appeared that alleviation of nighttime akinesia, reflected by the ability to turn around in bed, was perceived as the most worthwhile improvement.

The syndrome of acquired aphasia and convulsive disorders in childhood has received ample discussion since the initial description by Landau and Kleffner in 1957. Despite numerous investigations considering the linguistic and epileptic phenomena of the syndrome, the symptomatology still remains of a puzzling nature. Two aspects of the syndrome, the acquired nature of the aphasia and the type of linguistic symptomatology, have not been discussed thoroughly. In our case not only a history of developmental language pathology was present but language symptomatology also revealed a predominantly motor aphasia during a language deterioration phase. A careful review of the literature as presented here yields data in agreement with our findings. First we found further evidence in the literature that Landau-Kleffner's syndrome is not exclusively a primarily receptive language disturbance. Secondly, evidence in favour of a developmental type of Landau-Kleffner's syndrome was found in 25 additional cases. In this group of children with developmental language disturbances at least two distinct types seem to emerge. A group in which the already existing developmental language disturbances did not fluctuate during the course of the illness and a group in which a considerable deterioration of the developmentally disturbed language functions took place. The different patterns of language evolution not only seem to suggest the possibility of an acquired language pathology within a context of developmental language disturbances but also a congenital onset of the syndrome of Landau-Kleffner as the probable cause of developmental language pathology.

A review of the neurological complications presenting in uremia and an account of their presumed pathophysiology is given. With the introduction of different dialytic procedures during the last twenty years, the incidence and severity of neurological complications have declined. Nevertheless, some disturbances related to the uremic syndrome fail to respond to dialytic therapy and these therapeutic measures may even be responsible for the appearance of some new abnormalities. The clinical manifestations of uremic encephalopathy and polyneuropathy are presented. The review of the presumed pathophysiology of these syndromes illustrates the still existing controversies. Nevertheless, some promising new lines of research are reviewed. In addition, some complications of uremic treatment, including dialysis disequilibrium syndrome and dialysis encephalopathy are presented.