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End-of-life decisions in neurology have repeatedly given occasion for controversies. Often these are based on lack of knowledge of the juridical and ethical framework conditions. This review describes the juridical-ethical basis for the implementation and continuation, and for withholding and withdrawal of life-sustaining measures, in particular, the significance of medical indication and patient's will. The different forms of assisted dying ("Sterbehilfe"), namely homicide by request, assisted suicide, palliative symptom relief and treatment withdrawal are characterized. The "Principles of the German Medical Association" in end-of-life situations are illustrated. Specific features of neurological treatment scenarios are discussed such as the preclinical and clinical emergency and acute situation, the decompensation of stable chronic severe brain injury situations, and chronically progressive neurodegenerative diseases. In the latter situations, an early "Advance Care Planning" could contribute to improved end-of-life decision-making.

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Botulinum toxin poisoning has afflicted mankind through the mists of time. However, the first incident of food-borne botulism was documented as late as the 18th century, when the consumption of meat and blood sausages gave rise to many deaths throughout the kingdom of Württemberg in South Western Germany. The district medical officer Justinus Kerner (1786--1862), who was also a well-known German poet, published the first accurate and complete descriptions of the symptoms of food-borne botulism between 1817 and 1822 and attributed the intoxication to a biological poison. Kerner also postulated that the toxin might be used for treatment purposes. In 1895, an outbreak of botulism in the small Belgian village of Ellezelles led to the discovery of the pathogen "Clostridium botulinum" by Emile Pierre van Ermengem. Modern botulinum toxin treatment was pioneered by Alan B. Scott and Edward J. Schantz in the early 1970s, when the type-A serotype was used in medicine to correct strabismus. Other preparations of the type-A toxin were developed and manufactured in the United Kingdom, Germany, and China, whereas a therapeutic type-B toxin was prepared in the United States. To date, the toxin has been used to treat a wide variety of conditions associated with muscular hyperactivity, glandular hypersecretions and pain.

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Strokes have been known since ancient times. Today, stroke is the second most frequent cause of death and the most frequent cause of invalidity. In about 80% of cases, stroke is caused by cerebral ischemia and in about 20% by intracerebral hemorrhage, subarachnoidal hemorrhage, venous thrombosis and other cerebrovascular diseases. The brain is one of the most richly perfused tissues and depends fundamentally on the supply of oxygen and glucose. In order to assure adequate cerebral blood flow, the brain is capable of autoregulation through the interaction of diverse autoregulatory mechanisms (myogenic, neurogenic and metabolic factors, blood viscosity, renin-angiotensin-system and endothelium). Reduction of cerebral blood flow below the threshold of about 25 ml/100 g x min leads to an impairment of the functional metabolism and later to impairment of the structural metabolism. Pathophysiologically, a large number of isolated pathobiochemical processes (loss of energy, lactate acidosis, excitating amino acid release, ion balance disorders, calcium overload, free radical release, etc.) start to interfere with each other. Delayed edema and inflammation lead to secondary brain damage. Apoptosis is probably induced by ischemia and can cause secondary deterioration. The basic principles in the treatment of ischemia are firstly the rapid restoration of cerebral blood flow (lysis, carotid endarterectomy) and secondly--following infarction--a limitation of brain damage (preservation of ischemic but not necrotic brain tissue, prevention of secondary complications). Stroke treatment requires profound diagnostic and therapeutic expertise and interdisciplinary cooperation of neuroradiologists, neurosurgeons, vascular surgeons and cardiologists. Stroke can best be managed in special "stroke units", which have now been established in nearly all parts of Germany. Beside acute management of stroke and neurological rehabilitative treatment, emphasis has to be laid on primary (public information, education, treatment of risk factors) and secondary prophylaxis (treatment with antiaggregants, anticoagulants, a. o.).

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A growing number of patients with neuromuscular disease have been treated with home mechanical ventilation during the past 15 years. We prospectively examined the long-term effects and complications of this method, particularly with regard to noninvasive positive pressure ventilation (NPPV). Thirty-one patients with amyotrophic lateral sclerosis (ALS, n = 20) or other slowly progressive neuromuscular diseases (NMD, n = 11) were observed for 17,517 home ventilation days (almost 48 ventilation years). The mean observed ventilation time was 565 days (min/max: 30/2930). Twenty-five patients were ventilated noninvasively with different masks. The calculated mean survival with NPPV ventilation (criteria: death, tracheostomy, or patient deciding to break off) was 2052 (SE: +/- 317.8) days in the NMD group, 248 days (+/- 35.7) for ALS patients without bulbar symptoms, and 82 days (+/- 27.4) with bulbar paralysis. Complications with the need for intervention were observed six times more frequently with ALS than with NMD. NPPV is effective for years in patients with slowly progressing NMD. Those ALS patients without bulbar symptoms can profit for up to a year from NPPV, while those with bulbar paralysis can have some symptom relief. Complications of every kind are much more frequent in ALS patients.

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UNLABELLED: OBJECTIVE, PATIENTS, AND METHODS: A severe case of cerebral air embolism after unintentional central venous catheter disconnection was the impetus for a systematic literature review (1975-1998) of the clinical features of 26 patients (including our patient) with cerebral air embolism resulting from central venous catheter complications. RESULTS: The jugular vein had been punctured in eight patients and the subclavian vein, in 12 patients. Embolism occurred in four patients during insertion, in 14 patients during unintentional disconnection, and in eight patients after removal and other procedures. The total mortality rate was 23%. Two types of neurologic manifestations may be distinguished: group A (n = 14) presented with encephalopathic features leading to a high mortality rate (36%); and group B (n = 12) presented with focal cerebral lesions resulting in hemiparesis or hemianopia affecting mostly the right hemisphere, with a mortality rate as high as 8%. In 75% of patients, an early computed tomography indicated air bubbles, proving cerebral air embolism. Hyperbaric oxygen therapy was performed in only three patients (12%). A cardiac defect, such as a patent foramen ovale was considered the route of right to left shunting in 6 of 15 patients (40%). More often, a pulmonary shunt was assumed (9 of 15 patients; 60%). For the remainder, data were not available. CONCLUSION: When caring for critically ill patients needing central venous catheterization, nursing staff and physicians should be aware of this potentially lethal complication.

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We report about two female inpatients aged 58 and 24, suffering from non-purulent meningoencephalitis, in the first case caused by varizella-zoster-virus, in the second case probably due to viral infection. Both patients developed a diffuse brain edema associated with a progressive loss of consciousness. The adjunctive treatment with dexamethasone led to rapid improvement of clinical symptoms. Computed tomography revealed a significant reduction of brain edema. These results of these two cases support the efficacy of corticosteroids as adjunctive treatment of diffuse brain edema caused by non-purulent meningoencephalitis. The pathophysiological mechanisms are discussed.

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