With the development of selective methods of angiography and improvements in operative technique, accurate diagnosis and operative treatment of spinal angiomas have become possible to a greater extent.
In comparison with the opening discussion on the cerebral angiomas there seems to be no agreement so far on the indications and choices of operative procedure. The reason seems to be gene rally as yet scanty experience, the diverse clinical material and the different presentations in relation to the functional morphology and the pathogenesis of the medullary lesions. In practice one of the most important but unsatisfactory problems is the early diagnosis of the angiomas. I am reporting some of our own experipences in the hopes of answering some of these questions.

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Schistosomiasis of the spinal cord and especially of the conus and cauda is to the mind of the author not rare. The author′s collection of five cases in nearly two years is presented. All cases came to surgery and were verified histologically. Two were diagnosed preoperatively.
The literature on the subject is studied and presented. The mode of infestation of the spinal canal, the pathology, clinical picture and particularly the myelographic appearance are detailed. The value of serological tests is under study.
The author believes that the clinical and radiological features are so suggestive as to allow a more or less correct preoperative diagnosis. The patient is usually a boy between 10-20 years of age who comes suffering from low back and bilateral sciatic pains followed by the rapid onset of combined conus and cauda lesion with early onset and prominence of urinary incontinence. Evidence of bilharzial infestation in the urinary or intestinal tracts may be distincly lacking. Myelography reveals a localized block of the size of one vertebral body at the level of D12 or L1 having irregular often trifid edges and demonstrating abrupt intramedullary swelling.
A combination of pre-operative antibilharzial treatment and surgical decompression-with possible postoperative antibilharzial therapy especially if the condition is only recognised at operation-generally offers the best chances for cure. The prognosis in conus and cauda lesions is good.

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Optic nerve injury or blindness after head trauma has well been known since the days of Hippocrates, and has still remained one of the serious posttaumatic sequelae. Statistically about 2% of head-injured persons suffer from the visual loss and are impelled to have limited social activites³⁾. As the victims of traffic accidents are increasing every year, the studies about this problem are urgent.
Clinical manifestations of the injury of the optic nerve have been well known. The reports of many institutions have shown almost the same results. The summaries are as follows³⁾: There is a constant mode of trauma to make an injury. It occurs frequently in motorcycle accidents. Sometimes it occurs even in trivial accidents, where impact force is not always so large. The blow is usually given to the front of the head. Symptomatologically visual loss occurs immediately after the trauma and is limited usually to the eye on the ipsilateral side to the impact and spares the eye on the contralateral side. Diagnosis is guided from the loss of direct light reflex of the affected side. The fracture of the optic canal is often visualized in X-ray studies. Surgical intervention is not fully effective.
From the pathological view point, there are so many therories as to the causative factors of the injury of the optic nerve. The fracture of the optic canal, the bleeding of the sheath of the optic nerve, and the tearing of nerve fibers are prominent among them. Fracture theory seems most attractive because the fracture of the optic canal is found in 60-90% cases in X-ray studies.
So far, these clinical and pathological data have strongly suggested that mechanical factors play an important role to cause the lesion. However, there has never been a fundamental engineering study. Therefore in this paper, mechnical studies were performed to investigate the mechanism and to clarify the threshold of the impact force of the fracture of the optic canal, which is thought to be closely relevent to the ipsilateral optic nerve injury. The studies were made up of series of experiments.

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1) Four dry human skulls were statically compressed in fronto-occipital direction. The forces to produce bone fracture ranged between 600 and 1000kg weight. The load-deflection curves gave spring rates of 400 to 900kg/mm, average 600kg/mm.
2) Semi-free fall test to give impact on twenty dry human skulls at midfrontal regions were performed using a strain-gauge load cell, an accelerometer, DC amplifiers and a cathode-ray oscilloscope. Various buffer materials including the scalp simulator were used.
At fracture notching and abrupt lowering of the load curves as well as high frequency vibration of the acceleration curves were noted. The rise time at fracture became shorter compared to those when fracture did not occur. The dynamic load level for frontal bone fracture was between 400 and 1300kg, was independent of acceleration, energy, buffer materials as well as rise times. The peak loads at the moment of fracture were closely related to the weights of dry skulls. These results indicate that human skulls have the characteristics of brittle fracture both statically and dynamically.
3) Based on the above conclusions the tolerance limits against brain damage was theoretically considered and the Wayne State Human Tolerance Curve was criticized.
Postulating a head falling brow-down on a hard flat surface without the effect of the body, the threshold for fracture in terms of peak acceleration and rise time is very close to the Wayne State Human Tolerance Curve (H. T. C.). Above this threshold or even when higher energy is applied, the head does not give rise to a higher acceleration but fracture should occur at the same peak acceleration and possibly shorter rise time. This means transition to the safe zone of the H. T. C. Clinically, however, severer brain damage is expected. The H.T.C. and the pressure gradient theory due to translational acceleration should not be applied to brain damage in the presence of fracture. Instead, skull deformation and possibly snap-back of the deformed skull should be considered as the mechanism of the brain damage associated with skull fracture.

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Complete cerebral ischemia of 30min duration was produced in normothermic cats by clamping the innominate and the left subclavian arteries and simultaneously lowering the systemic blood pressure. After ischemia the brain were recirculated with blood for periods of 15 to 2hrs. The suppression and recovery of the neuronal function during and after ischemia were assessed in the sensorimotor cortex by recording the spontaneous EEG and the pyramidal response after stimulation of the cortex; by measuring the concentration of energy metabolites, such as phosphocreatine, adenosine triphosphate, glucose, and lactate, and by measuring the DNP-stimulated ATP-ase activity of isolated mitochondria in the brain. The EEG was suppressed 11±1.4 seconds after the onset of ischemia and the pyramidal response after 240±38 seconds. At the end of ischemia, the enregy rich phosphates were completely exhausted, the glucose content had fallen to 4% of the control value, and lactate increased 23 fold. The DNP-stimulated ATP-ase activity declined 22% of the control value. The ultrastructural alteration of the sensorimotor cortex was minimum at the end of ischemia.
Recovery of the pyramidal response started 3 to 6min after restoring the blood flow and was completed within 2hrs; the EEG reappeared after 1 to 2hrs. The functional recovery was related to the restoration of the energy rich phosphates and glucose-levels and to the simultaneous reduction of the accummulated lactate. Under the potimal conditions, CrP and glucose were normalized within 30min and lactate was reduced to 127% of the control value within 2hrs after the end of ischemia. The ATP concentration, and DNP-stimulated ATP-ase activity, however, returned only to 72% and less than 90% respectively, even when spontaneous EEG activity reappeared. The mitochondrial swelling which was observed as one of the structural changes of the sensorimotor cortex taken at this time, seemed to be related to the incomplete recovery of ATP concentration and DNP-stimulated ATP-ase activity.
The investigation of the clinical signs of the post-recirculation recovery of the cats was carried out only with conventional nursing of the postischemic animals and no complete recovery of the clinical signs could be observed in these animals.

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