To evaluate the neurotoxicity of paclitaxel/cisplatin chemotherapy, we studied neurological and electrophysiological functions in 14 patients who had been treated with 1–7 courses of paclitaxel/cisplatin. The cumulative paclitaxel and cisplatin doses ranged from 175 to 1225 mg/m2 and 100–700 mg/m2, respectively. Neurological examinations as well as motor nerve conduction studies of the peroneal nerve were performed and summarised by means of a peripheral neuropathy score. Neurotoxicity with onset usually after the second treatment cycle occurred in 13 patients. 12 patients complained about sensory symptoms, 13 patients had impaired vibration sense and 8 patients developed additional muscle weakness, predominantly of the legs. Dysfunction of peroneal motor nerve conduction occurred in 13 patients. Reduction of amplitudes as well as slowing of conduction velocities were seen in 13 patients and prolonged distal latencies in 10 patients. The peripheral neuropathy score was elevated in 13 patients. Neurological symptoms, impairment of both vibration sense and tendon reflexes, and the peripheral neuropathy score increased with the cumulative doses of paclitaxel/cisplatin. Serial analysis among selected patients also revealed an increase in neurotoxicity with increasing cumulative drug doses. These data indicate the development of neurotoxicity in most patients treated with paclitaxel/cisplatin and also suggest that early signs of neurotoxicity can be detected by clinical examination with emphasis on symptoms as well as vibration sense and can be well documented by electrophysiological investigations.

Bei Patienten mit koronarer bzw. peripherer Gefäßerkrankung ist das Risiko einer prophylaktischen Karotisendarterektomie wesentlich grōßer als bei klinisch Gesunden. Dieser Eingriff ist vor peripherer Gefäßrekonstruktion mit einer perioperativen Schlaganfalls-rate von etwa 5% und einer Mortalitätsrate von etwa 2% verbunden. Bei Patienten vor Koronararterien-Bypass-operation kommt es im Zusammenhang mit der prophylaktischen Karotisendarterektomie bei etwa 4% der Fälle perioperativ zu zerebralen Ischämien, zusätzlich besteht eine Mortalität von etwa 3%.

Bei 57 von 70 Patienten, die vor dem 40. Lebensjahr erstmals zerebrale Durchblutungsstörungen auf ischämischer Basis erlitten hatten, wurde der weitere Verlauf über durchschnittlich 84 Monate verfolgt. Innerhalb von 48 Monaten nach dem initialen Ereignis kam es bei 22 von 51 Patienten (43,1%) mit Spontanverlauf zu weiteren Manifestationen (Rezidivquote fur Patienten mit transitorischischämischen Attacken 78,6%, für Patienten mit prolongierten reversiblen Defekten 33,3%, für Patienten mit kompletten Schlaganfällen 28,6%), wobei 31,5% aller Patienten schon innerhalb des ersten Jahres neuerliche zerebrale Durchblutungsstörungen erlitten, die meisten sogar innerhalb der ersten wenigen Monate.

Within a period of 13 months a 24-year-old male student experienced four attacks of subarachnoid haemorrhage. An intradural-extramedullary haemangioma at the level of the second thoracic segment was found to be the cause of the repeated bleeding.

In this report we are describing 3 further cases of progressive supranuclear palsy, all displaying the typical clinical features (first described by Steele, Richardson and Olszewski, 1964): Ophthalmoplegia (affecting chiefly vertical gaze), pseudobulbar palsy, dysarthria, dystonic rigidity of the neck and upper trunk and dementia. Clinical symptoms started between 49 and 51 years of age with slow progression during 2 to 4 years. One patient died 2 years after the first clinical symptoms began. The purpose of this paper is, to describe a further group of 3 cases of progressive supranuclear palsy and to point out in detail the clinical symptoms, that all correspond to supranuclear localisation of this disease and to report about some differences in the development of the disease and the fully developed disorder. The use of treatment with Adamantin and Akineton was not (very) satisfying.

In this report we are describing 3 further cases of progressive supranuclear palsy, all displaying the typical clinical features (first discribed by Steele, Richardson and Olszewski, 1964): Ophthalmoplegia (affecting chiefly vertical gaze), pseudobulbar palsy, dysarthria, dystonic rigidity of the neck and upper trunk and dementia.