The operative procedures for ossification of the posterior longitudinal ligament (OPLL) of the cervical spine are mainly divided into two types, i.e., the posterior approach and the anterior approach. We conducted surgical treatment on about fifty cases of OPLL by the posterior approach until 1977. The results were mostly satisfactory for the spinal cord signs, but sometimes we could not improve the radicular signs. In addition, since ossification of the ligament continued to progress, we could do nothing about aggravation arising several years later. Therefore, we have tried a new and radical method which is called anterior decompression since 1978. The central part of the vertebral body and the ossified area of the posterior longitudinal ligament are removed and the defect is filled with a bonegraft. Twelve cases of OPLL were operated on in our department in the last two years. Surgical techniques, operative results and indications are discussed. A longitudinal groove of sufficient length and approximately 1.2-1.5 cm in width is made in the center of the vertebral bodies using a rongeur and an air-drill. When the posterior surface of the vertebral bodies is approached, the procedure should be performed with extra caution under a surgical microscope. The normal part of the dura must be exposed first, and the ossified ligament is carefully removed with a micro-rongeur. When the ossified ligament adheres tightly to the dura, the dura involved must be extirpated. The posterior part of the body should be cut widely so that the lateral part of the ossified ligament can be removed easily. A bone-graft taken from the iliac crest is made to fit the graft bed. The operative results were excellent even though the lateral parts of the ossified ligament were not removed completely in three cases and fracture of the grafted bone occurred in two cases. Marked improvements of radicular and spinal cord signs were seen in all twelve cases. There were no cases in which signs of aggravation of the neurological symptoms appeared after the operation. Three bodies fused in one case, four bodies in nine cases, and five bodies in two cases. The highest level of the fusion was C2 and the lowest level was T1. When the percent narrowing of the cervical spinal canal was over fifty percent and remarkable cord signs were present, there was a tendency for the improvement of the cord signs to be delayed. When there is a gait disturbance, the operation should be performed without hesitation. Theoretically, it is considered that any ossification of the ligament can be removed by the anterior approach as long as the number of vertebral bodies involved does not exceed five (C3 C7). Spinal CT scans were valuable and essential to obtain more detailed information about the stenotic spinal canal and shape of the ossified ligament.
Plasma α-fetoprotein (AFP) and human chorionic gonadotropin (HCG) concentrations were assayed in patients with intracranial teratomas or germinomas. Plasma AFP was significantly elevated in one patient with a yolk sac tumor, and in four with embryonal carcinomas, while in 14 patients with germinomas, the plasma AFP level was in the normal range. Plasma HCG concentrations were significantly elevated in two patients with embryonal carcinomas and in seven with germinomas. In one patient with a yolk sac tumor, the HCG concentration in CSF was elevated. Pertinent literature was reviewed and it was concluded that AFP is specific to yolk sac tumors and embryonal carcinomas, while HCG is common in all germinal tumors. Blood or CSF AFP and HCG are quite useful for detecting germinal tumors. They are also useful in evaluating the efficacy of the treatment.
Attempts were made to transplant five human brain tumors consisting of one meddulloblastoma, one anaplastic astrocytoma, one glioblastoma and two pituitary adenomas into hereditary asplenic-athymic (lasat) mice. One tumor line designated as KNS-GL-2 was established from the anaplastic astrocytoma. The tumor transplanted serially through two to four generations in lasat mice showed tumor growth in athymic nude mice as well and could be serially passaged. As the serial passage advanced, both the rate of tumor takes and the growth rate increased, and the tumor became more infiltrating. Tumors developed in mice showed good compatiblity with the original tumor in histological and ultrastructural characteristics in early passages of one to three generations, and immunoperoxidase positive tumor cells were identified in GFAP and S-100 protein preparations. Tumor cells with small, dark cytoplasm appeared in the third generation and they became predominant thereafter. Only the large and clear cells showed positive reactions in both GFAP and S-100 protein preparations. Dedifferentiation or malignant transformation by serial passage was suggested.
Plateau waves were produced experimentally during evoked sleep in cats and primates with kaolin-induced hydrocephalus. At the acute stage of hydrocephalus with moderate intracranial hypertention, Krebs-Ringer's solution containing excess calcium was perfused within the posterior region of the hypothalamus to induce sleep. Behavioral and physiological signs such as sleep were evoked within 5 to 30 min. following the start of perfusion, and lasted as long as 3 to 5 hours. When calcium ions had not sufficiently altered the arousal level of animals, sleep was induced by intravenous administration of a precursor of serotonin. In cats and primates with ICP raised above 15 mmHg, the ICP during induced sleep was exaggerated and developed plateau waves which had amplitudes of over 90 mmHg and durations of within 5 min. These plateau waves were highly reproducible. A relatively right situation of the intracranial space was a necessary condition for production of the plateau waves. The functional change in the hypothalamus involved in the sleep mechanism plays as an important role in formation of the plateau waves.
Orbital rhabdomyosarcoma in children is a relatively rare disease. There have been only 30 known cases reported in Japan. A case of orbital rhabdomyosarcoma with long-term survival was reported. An 11-year-old boy was admitted because of rapidly progressive exophthalmos, chemosis and visual disturbance of the right eye. Right carotid angiography demonstrated a walnut-sized tumor stained heterogeneously in the supero-lateral portion of the orbit which was fed by engorged external carotid branches as well as by the ophthalmic artery. A total removal of the tumor was performed through the frontozygomatic approach. Histological examinations revealed small cells with scanty cytoplasm distributed in the myxomatous matrix. Cross striations were stained in some tumor cells which had a long cytoplasmic process. He recieved 5, 500 rads by Linac irradiation postoperatively. His visual acuity improved from nearly blind to 0.15. Four years after the operation there is no sign of any tumor recurrence. It is very difficult to diagnose orbital rhabdomyosarcoma preoperatively because a definitive diagnosis must be based on histological findings. Cross striation which is often recognized in so-called racket cells with eosinophilic cytoplasm in light-microscopy and/or myofilaments in the tumor cells by electronmicroscopy are proof that the tumor is of myogenic origin.
To investigate whether the development of chronic subdural hematomas from posttraumatic subdural collections is a common occurrence, 40 cases of posttraumatic subdural collections of low density observed in two hospitals were followed with CT scans in the 30-month period between June 1, 1977 and Dec. 31, 1979. Their clinical courses were devided into three groups. (1) Among 40 patients with posttraumatic subdural collections of low density, eight subsequently developed chronic subdural hematomas. Five bilateral subdural collections evolved into bilateral chronic subdural hematomas. When the subdural collections were unilateral, the resulting hematomas developed at the site of the original collections. In five of these cases, CT scans at intermediate dates demonstrated a stage when the subdural collections had increased density but were not expanding. From these non-expanding subdural collections of increased density, expanding chronic subdural hematomas evolved in 2 weeks to 1 month. (2) In 10 cases, the subdural collections showed increased density at later dates but were eventually resolved without evolving into chronic subdural hematomas. (3) In the remaining 22 cases, the subdural collections were resolved without apparent increase in density. It was noted that the subdural collections remained at a uniformly low-density at least for the first month after the initial head injury and the increase in density occurred thereafter. The nature of these posttraumatic subdural collections of low density, which seem to be precursors of chronic subdural hematomas, are discussed. They appear to be posttraumatic subdural hygromas.
The authors reported a case of acute epidural hematoma which developed four hours after irrigation of the chronic subdural hematoma. A 56-year-old man was admitted. He was drowsy and disorientated with a one-month history of headache and dysarthria, but no other neurological deficits were noted. Laboratory data including bleeding and coagulating time, were all within the normal ranges. CT scanning and left carotid angiography showed a large left subdural hematoma. Irrigation of the subdural hematoma was performed the next day through two burr holes in the left fronto-parietal region under local anesthesia. About 150 ml of subdural hematoma was removed. Four hours after irrigation, he was semicomatose with right hemiplegia. CT scanning was immediately performed and reveled a epidural hematoma in the left parieto-occipital region. About 120 g of epidural hematoma was removed by left parieto-occipital craniotomy nine hours after the first operation. He gradually improved, and was discharged ambulant on the 51st postoperative day. The presumptive pathogenesis responsible for the development of the epidural hematoma in this case was bleeding from small dural vessels after detachment of the dura from the skull in the left parieto-occipital region. It was considered that the detachment occurred at the posterior burr hole in the beginning and was then accelerated by postoperative intensive evacuation of the hematoma through a closed-system drain.
Regional cerebral ischemia was induced in dogs by injecting a silicone rubber cylinder through the cervical internal carotid artery. The embolus was found to be lodged in the proximal portion of the middle cerebral artery in 33 dogs, distal portion of the middle cerebral artery in seven dogs, anterior cerebral artery in 11 dogs, posterior communicating artery in three dogs and osseous portion of the internal carotid artery in five dogs. Cerebral ATP and lactate and protein concentrations were quantitatively analysed in the parietal lobe, temporal lobe and basal ganglia of both the embolized and non-embolized hemispheres of each group. Relationships between the neurological signs and the changes in regional brain energy metabolism of each group were studied. In the group in which the embolus was lodged in the proximal portion of the middle cerebral artery, ATP depletion and lactate accumulation were most predominant in the basal ganglia of the embolized hemisphere. Disturbed consciousness and hemiparesis were observed. In the group in which the embolus was lodged in the distal portion of the middle cerebral artery, ATP depletion was evident only in the temporal lobe of the embolized hemisphere. Hemianopsia was observed in two of the three animals. In the group in which the embolus was lodged in the anterior cerebral artery, no neurological defect could be observed except in one animal showing disturbed consciousness and hemiparesis. This animal showed ATP depletion in the basal ganglia of the embolized hemisphere probably caused by obstruction of the perforating arterial branches from the anterior cerebral artery. In the group in which the embolus was lodged in the posterior communicating artery, protein concentration was decreased remarkably at all sites in the embolized hemisphere. It was considered to be acute brain swelling. Animals were comatose, and one of them died 3 hours after embolization. It was suggested that hypothalamus or posterior thalamus, the territory of the posterior communicating artery, might play an important role in causing acute brain swelling. In the group in which embolus was lodged in the osseous portion of the internal carotid artery, no neurological defect nor any change in energy metabolism could be seen. Regional energy metabolism was analysed 1, 3, 5, 12, 24 hours after embolization of the proximal middle cerebral artery. ATP levels in the basal ganglia of the embolized hemisphere which is the ischemic focus of this group decreased linearly up to 5 hours after embolization but were restored to the resting level 12 hours after embolization and were depleted again 24 hours after embolization. The transient restoration of the ATP values probably occurred because ischemic cell damage first took place at the site of ATP consumption such as a synapse rather than at the mitochondria where ATP was synthesized.