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Symptomatic cerebellar slump (CS) and external hydrocephalus (EH) are amongst the rarer complications of foramen magnum decompression (FMD) for Chiari I malformation (CM). CS typically presents with delayed onset headache related to dural traction or with neurological deficit offsetting the benefit of FMD. EH, consisting of ventriculomegaly along with subdural fluid collection(s) (SFCs), has been related to cerebrospinal fluid egress from a tiny breach in an otherwise intact arachnoid. We describe the case of a 21-year-old man with CM and syringomyelia who presented with impaired gag, spastic quadriparesis, and raised intracranial pressure 1 week following an uneventful FMD during which the arachnoid had been widely fenestrated. Magnetic resonance imaging (MRI) showed an infratentorial SFC, dilated aqueduct and triventriculomegaly, features of CS, and a residual but resolving syrinx. His symptoms resolved following a high pressure ventriculo-peritoneal shunt. At a 6-month follow-up visit, he was asymptomatic and demonstrated partial resolution of the syrinx, with no recurrence of the SFC. The unusual features in the clinical course of this patient were an atypical CS syndrome presenting with concomitantly resolving syringomyelia, and the development of EH after a wide arachnoidal fenestration. This is the first case in indexed literature describing such a combination of unusual postoperative complications of a FMD. A hypothesis is presented to explain the clinico-radiological findings of the case.

We would like to propose floating dural sac sign, which is observed as a hyperintense band or rim around the spinal dural sac on axial T2-weighted images, as a sensitive sign to identify cerebrospinal fluid (CSF) leakage. One hundred patients with orthostatic headache were prospectively registered in 11 hospitals. These patients were examined by brain magnetic resonance (MR) imaging (n = 89), radioisotope cisternography (n = 89), MR myelography (n = 86), axial T2-weighted imaging of the spine (n = 70), and computed tomography myelography (n = 2). In this study, we separately evaluated the imaging findings of intracranial hypotension and spinal CSF leakage. Among 100 patients, 16 patients were diagnosed as having spinal CSF leaks. Of 70 patients examined with axial T2-weighted imaging, 14 patients were diagnosed with spinal CSF leaks, and floating dural sac sign was observed in 17 patients, 13 patients with spinal CSF leaks and 4 without CSF leaks (sensitivity 92.9%, specificity 92.9%). Of 86 patients examined by MR myelography, extradural fluid was observed in only 3 patients (sensitivity 21.4%, specificity 100%). The floating dural sac sign was a sensitive sign that can be used to identify CSF leakage. Spinal axial T2-weighted imaging might be a good screening method for spinal CSF leakage that can help to avoid the need for lumbar puncture.

A 15-year-old girl developed a rare case of subdural hygroma after foramen magnum decompression for Chiari type 1 malformation manifesting as rapid symptom deterioration around 10 days after uncomplicated operation with uneventful immediate postoperative course. Progressive enlargement of the subdural hygroma in both supra- and infratentorial spaces was followed by the development of hydrocephalus. Syringomyelia improved shortly after the first operation but then deteriorated with massive presyrinx formation. Reoperation with wide opening of the arachnoid membrane lead to a rapid resolution of the hydrocephalus and the presyrinx. The present case shows that wide opening of the arachnoid membrane is an effective therapeutic option.

Two patients presented with spinal cerebrospinal fluid (CSF) leakage manifesting as chronic disabling headache and other symptoms after motor vehicle accidents. Combined radioisotope cisternography and computed tomography myelography confirmed the presence of the spinal leaks in the lumbar spine. Radioisotope cisternography has limited spatial resolution, so there is persistent and probably unfair mistrust in its reliability. The present 2 cases confirmed the diagnosis and support the causal relationship between motor vehicle accidents and spinal CSF leakage.

Acute subdural hematoma (SDH) is a rare but disastrous complication after lumboperitoneal shunt placement. Four of 206 adult patients with normal pressure hydrocephalus (1.9%) who underwent lumboperitoneal shunt placement suffered acute SDH following head trauma. The interval between shunt placement and acute SDH was one month to 7 years. Two patients had subdural effusion on computed tomography (CT) at 2- and 6-month follow up. All four patients required assistance in their daily activities before acute SDH onset. The traumatic event was a fall. On admission, CT revealed a large SDH that required surgical removal in two patients, of whom one had manifested subdural effusion after shunt placement. The other two patients had a small SDH. None of the four patients had cerebral contusions. Patients with lumboperitoneal shunts, especially those not capable of independent daily activities, are at risk for acute SDH after even minor head trauma.

A 37-year-old male and an 18-year-old male presented with spontaneous spinal cerebrospinal fluid (CSF) leakage from multiple nerve root sleeves. Both patients suffered abrupt onset of intense headache followed by nausea, dizziness, and one patient with and one without positional headache. Radioisotope spinal cisternography of both patients revealed that the CSF leaks were not localized in a special zone but distributed to multiple spinal nerve root sleeves. Magnetic resonance (MR) myelography suggested that the spinal CSF column was fully expanded to the root sleeves. The extraspinal nerve bundles demonstrated numerous high intensity spots. Both patients were treated conservatively, and their symptoms resolved within one month. Repeat radioisotope cisternography and MR myelography confirmed the spine was normal after recovery. We suggest that spreading disruption of the arachnoid membrane occurs at the nerve root sleeves due to CSF overflow into the spinal canal.

A 47-year-old man presented with chronic cranial subdural hematomas (SDHs) associated with spinal SDH manifesting as onset of severe lumbago revealed in the follow up for bilateral subdural effusions after trauma. Left chronic cranial SDH was first identified. Two months after evacuation of the left chronic cranial SDH, he complained of severe lumbago. Magnetic resonance imaging detected spinal SDH, prior to the diagnosis and treatment of right chronic cranial SDH. The present case of concomitant occurrence of cranial and spinal SDHs suggests that the possibility of spinal SDH should be investigated with magnetic resonance imaging in patients with chronic cranial SDH.

A 15-year-old boy presented with a case of middle cranial fossa arachnoid cyst associated with subdural effusion and manifesting as headache and vomiting after minor head injury. Computed tomography disclosed a cystic lesion in the left middle cranial fossa and ipsilateral subdural effusion. Fundoscopic examination revealed papilledema. A small tear of the cyst wall was confirmed endoscopically. Fenestration of the cyst was performed under the operating microscope. Postoperative course was uneventful. The tear in the outer wall of an arachnoid cyst may suggest the mechanism of occurrence of subdural effusion associated with middle cranial fossa arachnoid cyst.

Seven patients, six females and one male aged 26 to 39 years old, presented with headache in the upright posture, which was completely relieved in the recumbent posture. Radioisotope cisternography with technetium-99m-human serum albumin detected cerebrospinal fluid (CSF) leakage at the cervicothoracic level in six patients, and at the high cervical level in one patient. The diagnosis was intracranial hypotension due to spontaneous CSF leakage. Complete bed rest for more than 2 weeks resulted in complete resolution of the headache in all patients, and follow-up cisternography showed no leakage. Radioisotope cisternography is useful for the diagnosis of spontaneous CSF leakage, and complete bed rest for more than 2 weeks may be the best method of treatment.

A 56-year-old man developed subdural effusion after mild head trauma, which remained unchanged in volume and density on computed tomography during a follow-up period of 7 months. However, typical chronic subdural hematoma (CSDH) had developed by 9 months after the head trauma. The CSDH was successfully treated by irrigation and drainage. This unusually delayed onset of CSDH suggests that we should be aware of the possibility of very late onset of CSDH in patients with persistent asymptomatic subdural effusion.

The incidence of traumatic subdural effusion (TSE) was analyzed to clarify the relationship with subsequent chronic subdural hematoma (CSH) in 500 patients with head injury evaluated over a 36-month period. TSE occurred in 108 patients (21.6%), and CSH developed in 29 (5.8%) of these. The incidence of TSE was high, although only hospitalized patients were included because of the necessity for serial computed tomography. TSE frequently developed into CSH, and all CSH followed TSE. Therefore, TSE is closely associated with CSH and subdural effusion is probably a preliminary stage necessary for the formation of CSH.

A 70-year-old male presented with rapid neurological deterioration and fever 3 months after suffering a closed head trauma. He underwent craniotomy for possible subdural empyema based on computed tomography and clinical findings. Dural incision revealed an outer membrane typical of chronic subdural hematoma which covered a clear, yellowish fluid containing Campylobacter fetus. Histological examination confirmed the capsule of the hematoma, with a necrotic focus infiltrated by neutrophils. Administration of intravenous imipenem and topical tobramycin and cefalothin achieved total resolution of his neurological deficits. Development of the infected subdural effusion was probably secondary to bacterial infection in the pre-existing chronic subdural hematoma in the resolving stage. The presence of the hematoma capsule always carries the risk of development of an infectious focus.

A 57-year-old male developed subdural effusion after head trauma, which remained asymptomatic and unchanged in volume during a follow-up period of 3 months. A typical chronic subdural hematoma (CSDH) developed 6 weeks after burr-hole exploration in spite of the absence of hematoma capsule or blood components in the effusion. The CSDH was successfully treated by irrigation and drainage. This case suggests that the presence of blood in subdural effusion may be the trigger for evolution of CSDH. We recommend that asymptomatic subdural effusion should be followed up without surgical intervention.

A sequential study with computerized tomography (CT-scan) of two cases of chronic subdural hematoma was reported. Case 1 was a 67-year-old man who had a mild head injury. The initial CT-scan taken after 24 days of his injury showed bilateral frontotemporal extracerebral low density areas. This was diagnosed as subdural effusion because of its location, shape and the Hounsfield unit (11.0). He was admitted to our hospital with complaints of headache, nausea, vomiting and left hemiparesis. The CT-scan on the 41st day after his injury showed bilateral extracerebral high density areas instead of the previous low density. An operation was performed, and membranes of a subdural hematoma were observed. Case 2 was a 47-year-old man, who was admitted because of a mild head injury. The initial CT-scan (25 days) revealed bilateral extracerebral low density areas. This low density showed 11.7 in Hounsfield units suggesting subdural effusion. Follow-up CT-scans (after 76 days, 111 days, 113 days) demonstrated that chronic subdural hematoma had developed consequent on the post-traumatic subdural effusion. An operation disclosed a wellencapsulated hematoma. The conclusions obtained in this study were as follows; (1) Development of the hematoma membrane does not start immediately after head injury. (2) Subdural effusion is formed a few days after head injury. (3) Then, neomembrane begins to form during a certain period of subdural effusion. (4) Existence of the isolated cerebrospinal fluid between the dura and arachnoid membrane is the most important factor forming subdural hematoma. (5) Repeated hemorrhaging into the cavity from this neo-membrane may cause chronic subdural hematoma.

Excessive accumulation of CSF was found in the supratentorial intracranial extracerebral space of many infants by means of computerized tomography. CT head scanning was carried out 220 times in 153 clinically normal infants during the last year. The accumulation was most notable in the bifrontal convexity space, bitemporal convexity space, interhemispheric cistern, suprasellar cistern and Sylvian cistern. The space was not remarkable in new-born infants, but soon began to expand gradually until the infant became four months of age. The space was most remarkable four to seven months after birth. Then, the space decreased in volume gradually and disappeared between twelve and eighteen months of age, without any developmental, neurological or psychological troubles. Accidents during the fetal or delivery periods did not notably influence the with of the space. This phenomenon may be regarded as a physiological state in early infancy.

The authors report a case in which an enlarging skull fracture was surgically repaired on the fourth day after the initial injury. A 5-month-old boy fell from his father's arms and was hospitalized with a large, irregular protrusion in the left parieto-occipital region and right hemiparesis. Plain skull films showed a diastatic linear fracture with a maximum width of 8 mm, which expanded to 11 mm by the fourth day. Computed tomography (CT) scans revealed a cerebral contusion just beneath the fracture as well as a left subdural effusion. At operation, the contused brain tissue was found to have herniated over the bone defect. Craniotomy revealed a large dural defect, which was repaired with lyophilized dura. The patient was discharged with no neurological deficit. On the basis of a review of 58 recently reported cases of skull fracture, the authors conclude that the following conditions warrant consideration of early surgery: 1) a diastatic skull fracture with a width of at least 4 mm; 2) CT demonstration of a cerebral contusion beneath the fracture; 3) overlying scalp swelling; and 4) a neurological abnormality contralateral to the fracture. Performing surgery before the fracture gap becomes scalloped will result in more rapid neurological recovery and reduce the likelihood of enlargement of the fracture.

A case of cerebral fat embolism is reported. A 18-year-old patient with multiple bone fractures was in semicoma immediately after an injury. Brain CT showed no brain swelling or intracranial hematoma. Hypoxemia and alcoholemia were noted on admission, which returned to normal without improvement of consciousness level. In addition, respiratory symptoms with positive radiographic changes, tachycardia, pyrexia, sudden drop in hemoglobin level, and sudden thrombocytopenia developed. These symptoms were compatible with Gurd's criteria of systemic fat embolism. Eight days after injury, multiple low density areas appeared on CT and disappeared within the subsequent two weeks, and subdural effusion with cerebral atrophy developed. These CT findings were not considered due to cerebral trauma. Diagnosis of cerebral fat embolism was made. The subdural effusion was drained. Neurologic and pulmonary recoveries took place slowly and one month following the injury the patient became alert and exhibited fully coordinated limb movement. The CT scans of the present case well corresponded with hitherto reported pathological findings. Petechiae in the white matter must have developed on the day of injury, which could not be detected by CT examination. It is suggested that some petechial regions fused to purpuras and then gradually resolved when they were detected as multiple low density areas on CT. CT in the purpuras phase would have shown these lesions as high density areas. These lesions must have healed with formation of tiny scars and blood pigment which were demonstrated as the disappearance of multiple low density areas by CT examination. Cerebral atrophy and subsequent subdural effusion developed as a result of demyelination. The patient took the typical clinical course of cerebral fat embolism and serial CT scans served for its assessment.

Thirty cases of infantile traumatic subdural effusion were investigated to study the factors affecting it's clinical course, pathophysiology and prognosis. Although the clinical course of traumatic subdural effusion differs from case to case, it seems reasonable to classify it roughly into the following two types: (1) cases showing exacerbation of preceding chronic subdural effusion by head injury; and (2) cases with chronic subdural effusion or cases transformed from acute subdural effusion. These courses are intermingled with each other in some cases and the effect of treatment differs accordingly. The determining factors of the response to the treatment are numerous and interrelated. Among the various factors, the existing pathological changes in the cerebral parenchyma have the most serious effects. It is clinically important to establish the objective index predicting the prognosis before treatment. The accurate assessment of mental and physical development, measurement of cerebral hemodynamics and CT findings provide useful information for this purpose.

A case of aneurysm of vein of Galen in a 5½-month-old male baby is presented. The baby was born on February 16, 1978 and had apparently been well until age of 3 months, when he was suddenly seized with right hemiconvulsion. Positive findings on admission on Aug. 2, 1978 were setting-sun phenomenon, bulging of the anterior fontanel, equivocal weakness of the left lower limb, and bruit synchronous with pulsation on the scalp. The bruit was blowing, high-pitched and most prominent at the parieto-occipital region. CT scan disclosed an isodensity mass in the posterior part of the 3rd ventricle and symmetrical dilatation of the lateral ventricles. Cerebral angiography disclosed an enormously large aneurysm at the vein of Galen. Feeding arteries were the elongated and enlarged dural branch of the superior cerebellar artery on the right and bilateral medial posterior choroidal arteries. Draining veins were formed by huge straight sinus, basal vein, and dilated cortical veins. A right ventriculo-peritoneal shunt was placed for obstructive hydrocephalus prior to direct approach to the aneurysm. On August 25 and September 14, 1978, left temporal craniotomies were done. The clippings and divisions of the feeding arteries to the vein of Galen aneurysm were performed via subtemporal approach. The aneurysm completely disappeared on the postoperative angiography and an avascular mass was present between both posterior cerebral arteries. On clipping of a major feeder during general anesthesia, systemic blood pressure and central venous pressure suddenly elevated and bradycardia developed and lasted for 45 minutes. After recovery from anesthesia, atrial fibrillation suddenly developed. Suitable digitalization and preserving the hypovolemic state were successful to make the regular heart rhythm return. Variability of heart rate continued for about 24 hours thereafter. Postoperative CT scan and angiogram revealed bilateral subdural effusion. Repeated puncture and aspiration of the subdural fluid collection were performed but the fluid collection did not disappear. Postoperative PEG showed the patency of Sylvian aqueduct and no filling to the convexity subarachnoid space. Treatment of this subdural fluid collection still remains unsolved. This case is the third surgical case of aneurysm of vein of Galen to appear in the Japanese literature.

CT scans of 26 cases of subdural hematomas were carefully reviewed with particular emphasis on their densities. All the five cases of verified infantile chronic subdural hematoma, and four out of 15 cases of adult chronic subdural hematomas showed accumulations of CSF-dense fluid over the hemispheres, as well as in the cerebral sulci and cisterns, which were clearly demarcated from the overlying, rather highdense, subdural hematomas. The accumulation over the hemisphere was thicker where the underlying brain was severely atrophied. One of these had been erroneously diagnosed as ‘brain atrophy’. This and one adult case later progressed to a lentiform chronic subdural hematoma without CSF accumulation. Among six acute infantile subdural hematoma cases, three clinically mild cases showed accumulation of fluid in the sulci, fissures, and over the hemispheres, which gave the appearance of ‘brain atrophy’. Among three cases of severe form acute subdural hematomas, one showed a localized accumulation of CSF-dense fluid underneath the clot and over the hemisphere with sulcal patterns. In two cases of adult subdural effusions, metrizamide CT cisternography was performed. In both cases the dye not only filled the widely open cisterns and sulci, but also showed the existence of the subarachnoid space over the hemispheres and even beneath the subdural fluid space. From these observations it seemed logical that the subdural effusion (hematoma) was usually accompanied by enlargement of the subarachnoid spaces. In the acute phase, either primary subarachnoid hemorrhage or secondary bleeding from permeation of the subdural blood would cause blockage of the arachnoid villi, and the subsequent evolution of communicating hydrocephalus. In the chronic phase, however, hydrocephalus ex vacuo should play an important role, since the CSF accumulation appeared to have increased under decreased intracranial pressure with brain atrophy and/or enlargement of the calvarium, i.e., craniocerebral disproportion. Previous reports such as benign subdural collection of fluid, should be interpreted as the combination of subdural fluid with enlargement of the subarachnoid spaces. Similarly, in case termed benign enlargement of the subarachnoid spaces, benign communicating hydrocephalus, etc., the coexistence of subdural fluid must be considered and sought.

Diagnosis of posttraumatic subdural low density areas in computerized tomography (CT) has been quite controversial. Laboratory and in vivo CT analysis using the ACTA 0200FS were performed on 19 chronic subdural hematomas and five subdural hygromas. CT densities of the hematomas and of the ventricular CSF were obtained through regions of interest from preoperative plain CT scans. In six hematomas, both the supernatant and precipitant parts were separately sampled and the corresponding regions of interest were placed accordingly on the CT image. In these 25 hematoma samples, red blood cells (RBC), hematocrit, and hemoglobin (Hgb) varied greatly, though, these values correlated well with the CT densities. Plasma protein content was fairly constant with an average of 7.1±0.8 g/dl. Iron content was comparatively high, but still at levels negligible for CT density. There were four hematoma samples with RBC of less than 20×104 μl or Hgb of less than 2.0 g/dl. Their CT values ranged between 18 and 23 H.U., which were considered close to the in vivo serum level CT density. Five hygroma fluid showed no RBC and very little protein content of less than 0.4 g/dl. CT density ranged between -2 and 13 H.U.. One hygroma was so thin that placement of the region of interest was difficult. The edge effect of the skull was experimentally studied using a phantom skull filled with water. This revealed a remarkable overshoot of the CT values within ten pixels from the inner wall of the skull. Visual observation of the original CT pictures revealed four low density hematomas and seven mixed density ones. When compared to the density of the ventricular cavity, all of the low density hematomas and the supernatant part of the mixed density ones were clearly higher in density. All five hygromas appeared CSF dense or lower. Thus, visual observation offered clear distinction between hematoma and hygroma. In conclusion, because of the edge effect by the skull, thin subdural fluids could not be diagnosed by CT alone. Thick subdural fluids could be differentiated as either hematoma or hygroma by their CT densities. Subdural hematomas had in vivo CT densities of at least serum level or approximately 20 H.U., while subdural hygromas had densities close to CSF. These characteristics were best appreciated by visual observation of the CT scan films.

We attempted a pressure study of subdural fluid in 26 infant and child patients. The method used in the pressure study was as follows: a continuous recording was carried out with a polyethylene catheter inserted into the subdural fluid and connected to an externally placed pressure transducer and an amplifier chart recorder. The subdural pressure was measured by continuous recording over a period of 36 hours and then the subdural pulse waves were analyzed. The subdural mean pressures were classified into three patterns, namely A) continuous high pressure (more than 200 mm H2O), B) intermittent high pressure, and C) continuous low pressure (less than 100 mm H2O). Generally, both high pressure patterns were recognized in cases presenting light head injury or meningitis. Reexpansion of the brain was observed following surgical procedures in such cases. On the other hand the continuous low pressure pattern was observed in cases of brain atrophy following serious traumatic event and unknown etiology, and re-expansion of the brain was not obtained by surgical procedures. In analyzing pulse waves, polyphasic patterns were observed in cases of light traumatic event or unknown etiology. However, arch-like patterns were observed in cases where severe atrophic change of the brain occurred after various original diseases. The intracranial cavity contains three constituents, i.e., brain tissue, cerebrospinal fluid and blood. When the equilibrium of the three is disturbed, there is subdural collection of fluid to compensate for brain damage and changes in subdural pressure. We therefore consider measurement of subdural pressure and analysis of pulse waves to be significant in estimation of the degree of brain damage and to provide information for therapeutic indications.

Two cases of chronic subdural hematoma after craniotomy, removal of the hematoma, dural plasty using lyophilized human cadaver dura mater, and external decompression for acute traumatic intracranial hematoma are reported. One of these was acute subdural hematoma and the other acute epidural hematoma. The pathophysiology of the chronic subdural hematoma in these two cases was considered to be: collection of a mixture of cerebrospinal fluid and blood in the subdural space caused by torn arachnoid at head injury or craniotomy, and unbalanced volume between the brain and subdural space caused by excessive dural plasty and intracranial hypotension due to external decompression. Opening and irrigation of the hematoma cavity were sufficient treatment at cranioplasty.

The colloidal osmotic and hydrostatic pressure of chronic subdural hematomas were measured with a manometer in 35 patients. Manometric measurement showed an increase in the hematoma fluid corresponding to 5% of the total hematoma volume. The maximum colloidal osmotic pressure of the hematoma fluid, as measured with a transducer, was 23 ± 12 mmHg (mean ± standard deviation). Hemorrhage occurs continuously or intermittently within a subdural hematoma, accompanied by red cell hemolysis and hemoglobin degradation. The colloidal osmotic pressure within a subdural hematoma is higher than that in plasma or cerebrospinal fluid, so that the hematoma is able to absorb water through semipermeable membranes or capillaries. However, since the absorption force can transport only 5% of the hematoma volume, the colloidal osmotic pressure is a contributory process rather than a primary etiologic factor.