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"Traumatic late apoplexy" is a sudden cerebrovascular attack subsequent to traumatic cerebral lesion. According to Bollinger's concept, on which the term "traumatic late apoplexy" is based, this process was always a cerebral haemorrhage following trauma and appearing several days or weeks after the accident. In the discussions which followed after Bollinger had introduced this concept, the time sequence of this incident was fixed and the interval between trauma and apoplexy defined as occurring between the 6th day and the 8th week after the injury. However, cerebrovascular disease would have to be excluded; if this condition could not be verified with reasonable certainty, the patient would have to be at least less than 40 years of age. However, the pathological process always had to be "established" morphologically. This concept and this definition were extended a few decades later on the basis of progress made in the knowledge and treatment of cerebrovascular lesions. It was found that the pathological process need not be confined to haemorrhages only; every other traumatic cerebral lesion could be included which resulted in "apoplexy" in the clinical sense of the term with some delay after the trauma. Therefore, this article includes all modern concepts on such processes and discusses the various types of traumatic cerebral lesions which can occur in our present technological age. Reports published in literature are scrutinised and analysed more closely, and guidelines and hints are given which can be helpful in expertising work. The list of references is very extensive.

Unilateral embolization of the brain was performed in cats by intracarotid injection of 10.5 million carbonized microspheres (15 +/- 5 mu). Intracranial pressure increased from 6.1 +/- 1.5 to 14 +/- 2.3 mm Hg within two minutes and continued to rise more slowly to 24 +/- 18.3 mm Hg within four hours. Embolization caused a nonhomogenous distribution of microflow, but initially had no effect on global cerebral blood flow, nor on cortical oxygen tension. Yet, a functional suppression of cortical electrical and metabolic activity occurred. The ipsilateral EEG flattened irreversibly after 15 seconds; the contralateral EEG was transiently suppressed shortly thereafter. Arteriovenous difference of oxygen fell from 10.5 +/- 0.7 to 5.3 +/- 0.6 vol%, and the arteriovenous difference of glucose fell from 11.7 +/- 3.9 to 2.6 +/- 2.1 mg/100 ml as a consequence of reduced oxygen and glucose extraction. Subsequently, severe vasogenic brain edema, secondary ischemia, and severe functional suppression developed between two and four hours.

Cats underwent massive microembolization via carotid infusion of 10.5 million microspheres (15 +/- 5 mu in diameter), resulting in brain death within four hours; 87.4 +/- 10.2% of emboli reaching the brain were in the ipsilateral hemisphere; 87.9 +/- 4.4% were in the grey matter; and 12.1 +/- 4.4% were in the white matter. Evans blue and sodium fluorescein dyes were given intravascularly before and at different times after embolization. Fluorescence microscopy disclosed that embolization initially provoked a hyperemic engorgement of both the embolized and nonembolized hemispheres. Multifocal, blood-brain barrier extravasations occurred throughout the ipsilateral cortex and oral basal ganglia. Severe vasogenic brain edema ensued, with migration of extravasations from cortex into the white matter, which initially showed only minimal injury. Migration and accumulation of edema in white matter, with subsequent uptake and swelling of neuroglia and axons, may be related to secondary white matter damage following cortical embolic lesions. Degenerative foci developed throughout the embolized cortex over the one- to four-hour period of this study. These sites may correspond to those areas in which hyperemia and damage to the blood-brain barrier was present shortly after embolization.

The passage of contrast medium was observed using serial computed tomography (CT) in 24 stroke patients. Density--time profiles of various brain regions were plotted. In normal brain tissue, X-ray attenuation showed a maximum increase during the arterial phase (16.4 +/- 11.0%) and was 2.8 +/- 2.2% above control during stable distribution. In hypoperfusion, increase in attenuation was always below 10% in the arterial phase, while hyperperfusion was characterized by an attenuation increase of 25 to 70%. Enhancement was defined by a density increase of 16.8 +/- 14.8% and a tissue/blood ratio between 7 and 60%. An attempt was made to establish a relationship between the serial CT pattern and the prognosis. Enhancement tended to indicate severe morphological changes followed by permanent neurological deficit, whereas hyperperfusion was generally an indicator of probably recovery.

Localization of function in the brain is the attempt to correlate well-defined functions with circumscribed areas of the brain which can be characterized by their cytoarchitecture. The proof that such correlations exist and can be considered legitimate is demonstrated in the bedside neurologic diagnosis. This discussion, however, aims to show how many failures have already been made with this procedure and the still-existent dangers of repeating them.

The case of a stillborn full-term child is presented, which showed a fistsized supratentorial tumour. The origin of the anaplastic tumour from the ependymal surface is discussed. However, the mass remains an "Unclassified Tumour".

Cerebrovascular insufficiency arises from multiple causes, including cardiovascular insufficiency and local obstacles to the blood flow in the "four brain vessels". These obstacles are caused by primary thrombosis, by embolism, or by stenosing or ectatic arteriosclerosis. As there are anastomoses in the extra- and intracranial vessels, a collateral circulation can arise when hemodynamic conditions (blood pressure etc.) are adequate; this is also necessary for the preservation of these collaterals in later stages. Since particular hemodynamic conditions (terminal and watershed zones) have particular roles, different patterns of infarction can arise. Local obstacles to the blood flow can be subjected to vascular surgery as a preventive measure or even for vital conditions. The details of cerebral blood flow and brain viability have not become completely clear from the results of modern experimentation. The setting up of research institutes to concentrate on arteriosclerosis and ischemia in collaboration with clinical centers devoted to coronary and cerebral infarction seems to be very necessary.

The antitumor agent chloroethylcyclohexyl-nitrosourea (CCNU) was examined using a rat glioma model. A i.p. administration of three times 40 mg/kg CCNU was highly effective and increased the life-span of tumor-bearing rats from 53 to 86%. A total quantity of CCNU amounting to less than 30 mg/kg was not effective. On the other hand, large dosages exceeding LD10 proved to be toxic. The depression of platelets and white blood cells was mild after a single dosage of 40 mg/kg CCNU which recovered on about the 6th day. In the CCNU-treated animals there was an increase of the extent of necrobiosis. Ballooning of tumor cells with nuclear pyknoses and a lack of mitotic features occurred. Microcystic changes appeared sometimes to be more frequent than in control groups.

The data about the arterial spinal circulation in man are presented, some spinal syndromes "unexplained still today" in their pathogenesis are described, and the earlier attempts to formulate working hypotheses for the explanation of this spinovascular insufficiency are critically rediscussed.

Moderate unilateral cerebral ischemia was produced by microembolism in 24 adult cats. Two million plastic microspheres with a diameter of 15 +/- 5 microns were injected into the left common carotid artery via the lingual artery. The physiological and metabolic responses to embolism were accessed by electrocorticography and by determining the cerebral energy state. Embolism caused an immediate slowing and voltage reduction of the ipsilateral electrocorticogram with a gradual recovery after 30 to 60 min. Some animals also had an immediate and short depression of the contralateral electrocorticogram. In spite of the market functional suppression, metabolites of the cerebral energy-producing metabolism in most of the animals changed only slightly. In the embolized hemisphere pyruvate increased from 0.06 to 0.10 mumol/g and lactate from 1.9 to 4.6 mumol/g within 5 min after embolization and remained at this level during the 4 h observation period. Phosphocreatine, adenosine triphosphate and the energy charge of the adenylate pool remained uncharged during this period. However, there was a slight increase of ATP in the non-embolized hemisphere during the early postembolic period. In two animals, the initial slowing of the electrocorticogram recurred and spread to the contralateral hemisphere, followed by bilateral flattening after a few hours. This delayed functional deterioration was accomplished by complete loss of energy-rich phosphates. These animals also had a progressive increase of cerebrospinal fluid (CSF) pressure and considerable brain swelling with cerebellar herniation after 4 h. It is concluded that unilateral cerebral embolism in the above concentration leads only to a slight increase of anerobic glycolysis without significant perturbation of the cerebral energy state, unless progressive brain swelling with cerebrellat herniation supervenes. This supports previous findings, that brain edema and not initial ischemia is the main pathogenetic factor for tissue damage in cerebral microembolism.

To date a few clinical methods give a certain hint as to the presence of brain edema and even its most probable localization; only one method, the recently developed computer tomography can be regarded as fairly reliable. However, as long as the pathogenesis of brain edema is not yet sufficiently elucidated and therapeutic methods are not developed either to prevent or remove intra-or extra-cellular edema distinctly and separately in experimental lesions, the lack of adequate technology for a refined diagnosis in the human is not urgent.

Subcutaneously and intracerebrally transplanted neurinomas as well as intracerebrally grafted gliomas, both derived from primary tumors with resorptive carcinogens were investigated after injection of micropaque by conventional histologic methods and by postmortem X-ray analysis. Growth pattern and vasculature were similar in subcutaneously and intracerebrally transplanted malignant neurinomas. The most common feature was a parallel arrangement of vessels as shown by microradiography and vessel free zones. In intracerebrally grafted glioma, the growth of tumors was confined to or starting from the ventricular system. Sinusoidal vessels, capillary proliferations and proliferation of vessel wall were found. The outstanding feature was the occurrence of extravascular contrast deposits, thus indicating the vulnerability of tumor vessels and frequency of hemorrhages into these tumors.

102 patients entered a multicentric randomized study from May 1978 till December 1980. After an operative removal of a supratentorial astrocytoma grade 3 or 4 all patients were treated by radiotherapy of the whole brain with 40 Gy, and after a rest of 1 to 2 weeks with a boost dose of 20 Gy to the tumor region. By randomization the patients got misonidazole (400 mg/m2) to each of the 30 fractions or a placebo. The overall tolerance was good. A mild transient peripheral neuropathy was seen only in 2 patients. The median of survival time was not significantly different for both groups with 16 months (grade 3) and 10 months (grade 4). Thus a radiosensitizing effect of misonidazole was not proven.

Space-occupying lesions occurring in the spinal cord, its covers and in the neighbouring vertebral column are reviewed with consideration to their favourite site and the patients age and sex. The main tumor types are described with special reference to the literature and a comparison is made to the findings of specific tumors when occurring intracranially.