T Kawamata

Nihon University, Edo, Tōkyō, Japan

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Publications (56)92.7 Total impact

  • Neurologia medico-chirurgica 01/2012; 52(1):1-30. · 0.49 Impact Factor
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    ABSTRACT: The retrosigmoid intradural suprameatal approach with the patient in a semisitting position is an effective alternative to transpetrosal approaches for the treatment of petroclival meningiomas. The authors have made a simple modification to the retrosigmoid intradural suprameatal approach by using the lateral oblique position and preferentially dividing the tentorium with limited drilling of the suprameatal bone, which is termed the "lateral supracerebellar transtentorial approach." Twenty-six patients with petroclival meningiomas surgically treated via the lateral supracerebellar transtentorial approach were analyzed. All tumors had most of their bulk in the posterior fossa with some degree of extension into the middle fossa and/or Meckel cave. The patient is placed in the lateral oblique position, and a standard retrosigmoid craniotomy is performed. The tentorium medial to the trigeminal nerve is incised toward the free edge, which improves exposure to the petroclival region without extensive resection of the suprameatal petrous bone. Gross-total resection was achieved in 11 patients (42%). Ten patients (38%) underwent subtotal resection, and 5 patients (19%) underwent partial resection. There was no incidence of operative death, and the postoperative permanent morbidity rate was 15%. All patients except one did well postoperatively and were independent at the time of their last follow-up examinations. The lateral supracerebellar transtentorial approach provides the simplest and safest access to the petroclival region. It offers an advantageous approach to petroclival meningiomas exclusively located in the posterior fossa with minimal extension into the Meckel cave and middle fossa.
    Journal of Neurosurgery 03/2011; 115(1):49-54. · 3.15 Impact Factor
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    ABSTRACT: Age is an important factor influencing outcome after severe traumatic brain injury (TBI). In general, the older the victim, the higher the probability of a poor outcome. To investigate the mechanism underlying the link between age and outcome, the data for 797 patients enrolled in the Japan Neurotrauma Data Bank (JNTDB), aged 6 years or older, with Glasgow Coma Scale (GCS) scores of 8 or less on admission or deterioration to that level within 48 h of impact were analyzed. Thirty-eight percent of the patients were between the ages of 40 and 69 years, and 24% of the patients were older than 69 years. Older patients had higher rates of mortality and lower rates of favorable outcome. The frequency of mass lesions which were associated with poorer outcomes significantly increased with age, but regardless of the intracranial lesion type, older patients had poorer outcomes. The GCS score and the occurrence of systemic complications did not differ significantly according to age. Multiple systemic injury was less frequent in older patients. The varied occurrence of intracranial lesion types according to age is likely caused by the disparity between the young and aged brain in the progression of secondary brain injury. Alteration in the pathophysiological response, which is related to the development of secondary brain injury in the aging brain, probably contributes to more severe and irreversible brain damage in older patients, and is thus associated with poor outcomes.
    Journal of Neurotrauma 01/2009; 25(12):1407-14. · 4.30 Impact Factor
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    ABSTRACT: In this study, we examined the age-associated defect of stromal cells, which support B cell development, treated with 5-fluorouracil (5-FU) to induce severe perturbation of hematopoiesis, including B lymphocyte development, using SAMP1 mice exhibiting senescence-mimicking stromal-cell impairment after 30 weeks of age. Significant findings of this study are as follows: first, a marked and prolonged decrease in number of CFU-preB cells in non-SCI mice (58% of the steady-state level) associated with more markedly depressed number of CFU-preB cells in SCI mice (20% of the steady-state level), despite the absence of difference in the number of CFU-GMs during the period; second, in the non-SCI mice, a significant and prolonged up-regulation of GM-CSF and IL-6, positive regulators of myelopoiesis and suppressive factors of B lymphopoiesis, was observed. In SCI mice, greater and prolonged suppression of B lymphopoiesis was clearly demonstrated by the significant up-regulation of the negative regulator TNF-alpha associated with the concomitant marked down-regulation of the positive regulator SDF-1, although the increases of GM-CSF and IL-6 were limited. That is, 'negative complementation' makes preB recovery after 5-FU treatment impaired and prolonged. Principal component analysis clearly showed differences in the cytokine expression patterns in both early and later phases and the time course of the expression pattern of each cytokine between SCI and non-SCI mice without supervising information. An impaired regulation of the expressions of not only positive but also negative regulators after 5-FU treatment was, in part, the cause of the impaired regeneration of CFU-preB cells in SCI mice.
    Journal of Applied Toxicology 03/2008; 28(6):797-805. · 2.60 Impact Factor
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    ABSTRACT: We present here the first report of a jugular bulb venous thrombosis after mild head injury, which lacked either a skull fracture or abnormal findings on CT scan. An 8-year-old boy was hit on the back of the head and experienced headache and vomiting beginning the next morning. A CT scan and cranial x-ray examination failed to reveal any abnormal findings. The patient was treated conservatively; however, his headache and vomiting persisted. At 13 days after the injury, he began to show double vision due to left VIth nerve palsy and bilateral papilloedemas, suggesting an increased ICP. Although repeated CT scan failed to detect abnormal findings in both the supra- and infra-tentorial regions, MRI clearly visualized a thrombus which was situated within the right jugular bulb. Furthermore, MRV demonstrated disruption of venous flow at the jugular bulb. The patient was administered heparin continuously. His symptoms improved and the CSF pressure on lumbar puncture returned to a normal level at 20 days after admission. Magnetic resonance imaging showed resolution of the clot, and MRV appeared to demonstrate partial recanalization simultaneously. The patient was discharged without any neurologic deficits. The clot in the jugular bulb disappeared completely after 4 months, and he could be followed up for 1 year. This case underscores the fact that MRI may represent the exclusive screening examination in cases of sinus thrombosis when it occurs within the jugular bulb, as CT scan fails to reveal any findings suggestive of venous thrombosis.
    Surgical Neurology 01/2008; 68(6):660-4; discussion 664. · 1.67 Impact Factor
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    ABSTRACT: Symptomatic cerebral vasospasm is a major complication in patients with subarachnoid hemorrhage (SAH). Symptomatic cerebral vasospasm has been reported to be related to the patient's blood volume which is influenced by cerebral salt wasting syndrome (CSWS). We undertook a prospective study to assess whether the onset of symptomatic cerebral vasospasm was predictable or not, by observing the phenomena of CSWS (natriuresis and osmotic diuresis). Sixty-seven consecutive aneurysmal SAH patients were analysed. After surgery, all patients underwent hypervolemic therapy in order to keep central venous pressure (CVP) within 8-12 cmH(2)O, serum sodium level above 140 mEq/l and a positive water balance. Patients were classified into two groups: those without symptomatic cerebral vasospasm (n=55) and those with symptomatic cerebral vasospasm (n=12). To estimate natriuresis and osmotic diuresis, sodium in/out, water in/out, CVP and other parameters were measured and compared between the two groups. One day before symptomatic cerebral vasospasm, three factors reached statistical difference in the group that experienced symptomatic cerebral vasospasm: sodium balance, urine volume and water balance. On the day of symptomatic cerebral vasospasm, two factors reached statistical difference: sodium excretion and urine volume. No factor was significantly different 2 days before symptomatic cerebral vasospasm. Symptomatic cerebral vasospasm has a strong relationship with CSWS. Negative sodium and water balance and increased urine volume indicate a predictor of symptomatic cerebral vasospasm. To predict symptomatic cerebral vasospasm, strict observations are required, because CSWS and symptomatic cerebral vasospasm which follows, develop rapidly.
    Neurological Research 01/2008; 29(8):835-41. · 1.18 Impact Factor
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    ABSTRACT: BackgroundCerebral salt wasting (CSW) frequently occurs concomitantly with aneurysmal subarachnoid haemorrhage (SAH). CSW induces excessive natriuresis and osmotic diuresis, and reduces total blood volume. As a result, the risk of symptomatic cerebral vasospasm is elevated. Therefore, we investigated the relationship between the amount of bleeding, the intensity of CSW, and the diameter of the middle cerebral artery (MCA). MethodMale Wistar rats were used. The EP and BI models were produced by endovascular puncture of the intracranial artery and by autologous blood injection into the cisterna magna, respectively. To evaluate CSW, urine was cumulatively collected from SAH onset to 6 h later and sodium excretion was analyzed. We classified SAH on the basis of the amount of bleeding in the subarachnoid space. FindingsIn the EP model, the grade of SAH was directly proportional to urine volume and sodium excretion (P<0.01). The diameter of MCA in SAH rats was smaller than in EP-sham rats (P<0.01). However, the BI model had no difference in urine volume and sodium excretion. ConclusionsThe EP model is a suitable model for the study of CSW, concomitant with natriuresis and diuresis after SAH. The cause of CSW may not be the amount of bleeding.
    12/2007: pages 367-370;
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    ABSTRACT: Hyponatremia is a frequently observed electrolyte abnormality in patients with central nervous system disease. Several mechanisms, such as SIADH, hypopituitarism, and CSWS, have been proposed with varied incidences among several studies. We attempted to clarify the incidence and mechanism of hyponatremia for each type of TBI. We also assessed the efficacy of sodium supplementation and retention therapy. For sodium retention therapy, hydrocortisone was administered, expecting its mineralocorticoid effect, when the hyponatremia was associated with excess natriuresis. Retrospective analysis of 298 patients with TBI between January 2003 and December 2004 was performed. The incidence, background, clinical data, and outcome were evaluated. Of the 298 patients, 50 (16.8%) presented hyponatremia during the time course. Hyponatremia was associated with longer hospital stay (P < .001) and bad outcome (P = .02). Among these 50 patients, 37 recovered from the hyponatremia with simple sodium supplementation. The remaining 13 patients presented massive natriuresis and required additional sodium retention therapy. Hydrocortisone statistically reduced the amount of sodium excretion (P = .002) and returned the serum sodium level to a normal value. A high rate of hyponatremia after TBI was observed. Further studies are required to establish the precise mechanism of hyponatremia after TBI. Clear definition of CSWS is required to avoid confusion of the pathophysiology that causes hyponatremia. Hydrocortisone was useful to prevent excess natriuresis.
    Surgical Neurology 11/2007; 68(4):387-93. · 1.67 Impact Factor
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    ABSTRACT: Hyponatremia is common after aneurysmal subarachnoid hemorrhage (SAH). It is caused by natriuresis, which induces osmotic diuresis and decreases blood volume, contributing to symptomatic cerebral vasospasm (SCV). Hypervolemic therapy to prevent SCV will not be efficient under this condition. We conducted a randomized controlled trial to assess the efficacy of hydrocortisone, which promotes sodium retention in the kidneys. Seventy-one SAH patients were randomly assigned after surgery to treatment with either a placebo (n=36) or 1200 mg/d of hydrocortisone (n=35) for 10 days and tapered thereafter. Both groups underwent hypervolemic therapy. The primary end point was the prevention of hyponatremia. Hydrocortisone prevented excess sodium excretion (P=0.04) and urine volume (P=0.04). Hydrocortisone maintained the targeted serum sodium level throughout the 14 days (P<0.001), and achieved the management protocol with lower sodium and fluid (P=0.007) supplementation. Hydrocortisone kept the normal plasma osmolarity (P<0.001). SCV occurred in 9 patients (25%) in the placebo group and in 5 (14%) in the hydrocortisone group. No significant difference in the overall outcome was observed between the 2 groups. Hydrocortisone overcame excess natriuresis and prevented hyponatremia. Although there was no difference in outcome, hydrocortisone supported efficient hypervolemic therapy.
    Stroke 09/2007; 38(8):2373-5. · 6.16 Impact Factor
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    ABSTRACT: Nasal dermal sinus-cyst (NDSC) is a rare abnormality consisting of a dermal sinus opening at the nasal skin and dermoid cyst localized in the frontobasal area. A 2-year-old boy was admitted to our hospital due to swelling of the fronto-nasal regions with pus running from an orifice situated in the nasal skin. Bone-image CT and 3D-CT revealed bone defects within the frontal skull base. MRI demonstrated that a dermoid cyst centered in a bone defect was in contact with the dura of the frontobasal area, and a dermal sinus extending to the frontonasal skin could also be detected. Surgical resection was performed by frontobasal craniotomy. The dermal sinus was followed subcutaneously into the orifice of the nasal skin. A small skin incision was made and the sinus was then totally removed. The authors describe in detail this case of NDSC which extended to the intracranium, and review the literature regarding this abnormality.
    No shinkei geka. Neurological surgery 02/2007; 35(1):71-6. · 0.13 Impact Factor
  • Tatsuro Kawamata, Yoichi Katayama
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    ABSTRACT: The early massive edema caused by severe cerebral contusion results in progressive intracranial pressure (ICP) elevation and clinical deterioration within 24-72 h post-trauma. Surgical excision of the necrotic brain tissue represents the only therapy, which can provide satisfactory control of the elevated ICP and clinical deterioration. In this chapter, we review the results of our clinical studies regarding the pathophysiology of contusion edema and evaluate the effects of surgical treatment, i.e. contusion necrotomy, by analyzing the data from the Japan Neurotrauma Data Bank.
    Progress in brain research 02/2007; 161:235-41. · 4.19 Impact Factor
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    ABSTRACT: Severe cerebral contusion is often associated with nonhemorrhagic mass effect that progresses rapidly within 12 to 48 hours posttrauma. The mechanisms underlying such a rapid progression of mass effect cannot be fully explained by classic concepts of vasogenic and cytotoxic brain edema. Data from previous clinical trials, including diffusion-weighted magnetic resonance imaging studies, have indicated that cells in the central (core) area of the contusion undergo shrinkage, disintegration, and homogenization, whereas cellular swelling is located predominately in the peripheral (rim) area during this period. The authors hypothesized that high osmolality within the contused brain tissue generates an osmotic potential across the central and peripheral areas or causes blood to accumulate a large amount of water. To elucidate the role of tissue osmolality in contusion edema, they investigated changes in tissue osmolality, specific gravity, and ion concentration in contused brain in both experimental and clinical settings. Their results demonstrated that cerebral contusion induced a rapid increase in tissue osmolality from a baseline level of 311.4 +/- 11.3 to 402.8 +/- 15.1 mOsm at 12 hours posttrauma (p < 0.0001). Specific gravity in tissue significantly decreased from 1.0425 +/- 0.0026 to 1.0308 +/- 0.0028 (p < 0.01), reflecting water accumulation in contused tissue. The total ionic concentration [Na+] + [K+] + [Cl-] did not change significantly at any time point. Inorganic ions do not primarily contribute to this elevation in osmolality, suggesting that the increase in colloid osmotic pressure through the metabolic production of osmoles or the release of idiogenic osmoles can be a main cause of contusion edema.
    Neurosurgical FOCUS 01/2007; 22(5):E5. · 2.49 Impact Factor
  • Tatsuro Kawamata, Yoichi Katayama
    No shinkei geka. Neurological surgery 07/2006; 34(6):567-75. · 0.13 Impact Factor
  • T Kawamata, Y Katayama
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    ABSTRACT: Early massive edema caused by severe cerebral contusion results in elevation of intracranial pressure (ICP) and clinical deterioration within 24-72 hours post-trauma. Previous studies indicate that cells in the central area of the contusion undergo shrinkage, disintegration, and homogenization, whereas cellular swelling is predominant in the peripheral area, suggesting that early massive edema is attributable to high osmolality within necrotic brain tissue and may generate an osmotic potential across central and peripheral areas. We analyzed the effects of surgical excision of necrotic brain tissue in 182 patients with cerebral contusion registered with Japan Neurotrauma Data Bank; 121 patients (66%; Group I) were treated conservatively, and 61 (34%; Group II) were treated surgically. Most Group II cases (90%) underwent complete excision of necrotic brain tissue and evacuation of clots. Group I demonstrated higher mortality at 6 months post-trauma compared to Group II (48%) vs. 23%; p = 0.0001; n = 182). Striking differences were observed in patients scoring 9 or more on Glasgow Coma Scale at admission (56% vs. 17%); p = 0.017; n = 45) and demonstrated "talk-and-deteriorate" (64% vs. 22%: p = 0.026; n = 29), supporting our hypothesis that early massive edema is caused by cerebral contusion accompanied by necrotic brain tissue, indicating that surgical excision of necrotic brain tissue provides satisfactory control of progressive elevation in ICP and clinical deterioration in many cases.
    Acta neurochirurgica. Supplement 02/2006; 96:3-6.
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    ABSTRACT: Matrix metalloproteinases (MMPs) are associated with blood-brain opening and may be involved in the pathophysiology of acute brain injury. Previous research demonstrated that knockout mice deficient in MMP-9 subjected to transient focal cerebral ischemia had reduced blood-brain barrier (BBB) disruption and attenuated cerebral infarction. In this study, we examined MMP-9 up-regulation, BBB disruption, and brain edema formation after cortical impact injury in rats. Cortical contusion was induced by controlled cortical impact. Animals were sacrificed at intervals after injury. MMP up-regulation was assessed by gelatin zymography, and BBB integrity was evaluated using Evans blue dye with a spectrophotometric assay. Brain water content was measured by comparing wet and dry weights of each hemisphere as an indicator of brain edema. Zymograms showed elevated MMP-9 as early as at 3 hours after injury, reaching a maximum at 18 hours. Peak levels of BBB disruption occurred 6 hours after injury. Brain edema became progressively more severe, peaking 24 hours after injury. Compared to control group, treatment with MMP-inhibitor GM6001 significantly reduced BBB disruption 6 hours and brain water content (85.9 +/- 0.5% vs. 82.6 +/- 0.3%; p < 0.05) 24 hours after injury. These findings suggest that MMP-9 may contribute to BBB disturbance and subsequent brain edema after traumatic brain injury.
    Acta neurochirurgica. Supplement 01/2006; 96:130-3.
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    Neurotraumatology. 11/2005; 28:85-88.
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    ABSTRACT: Hyponatremia is a common complication in patients with aneurysmal subarachnoid hemorrhage (SAH). Such patient demonstrates excessive natriuresis and an increased risk of symptomatic cerebral vasospasm. However, the precise mechanisms underlying SAH induced hyponatremia remain unclear. In the present study, in order to establish an experimental model of hyponatremia following SAH, we induced SAH in rats, and evaluated the serum sodium (Na) levels, Na excretion and physiological parameters. Twenty-four male Wistar rats were used. SAH was induced by an endovascular puncture method. The mean arterial pressure (MAP), intracranial pressure (ICP), and cerebral blood flow (CBF) were monitored continuously. The urine was collected cumulatively for 12 hours after SAH, and the urine Na concentration was determined with a spectrophotometer. The serum Na levels were measured at 12 hrs, 2 and 4 days following the SAH induction. The mean (+/- standard deviation) baseline ICP was 3.5 +/- 2.6 mmHg, and increased to 67.4 +/- 17.6 mmHg immediately following induction of SAH. CBF decreased rapidly, and then gradually recovered to 70-80% of baseline. The urine volume and total Na excretion were significantly increased in comparison to those of the sham (P < 0.05). The serum Na level was significantly decreased at 4 days following SAH (P < 0.05). The present results demonstrated for the first time that rats with SAH exhibited excessive natriuresis. The endovascular puncture model is suitable for investigating hyponatremia that occurs concomitantly with natriuresis and diuresis after SAH.
    Acta neurochirurgica. Supplement 01/2005; 95:377-80.
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    ABSTRACT: Hyponatremia caused by excessive natriuresis is common in patients with aneurysmal subarachnoid hemorrhage (SAH). Natriuresis decreases the total blood volume through osmotic diuresis and increases the risk of symptomatic cerebral vasospasm. In such patients, hypervolemic therapy is difficult to achieve without causing hyponatremia because sodium replacement provokes further natriuresis and osmotic diuresis. We examined the effects of hydrocortisone, which promotes sodium retention, in patients with SAH. Twenty-eight SAH patients were randomized into 2 groups after direct surgery: group 1 patients without hydrocortisone treatment (n=14) and group 2 patients with hydrocortisone treatment (1200 mg/d for 10 days; n=14). Both groups underwent hypervolemic therapy by aggressive sodium and water replacement. The goal of the hypervolemic therapy was to maintain the serum sodium level >140 mEq/L and the central venous pressure (CVP) within 8 to 12 cm H2O. Group 2 demonstrated a lower sodium excretion (P<0.05) and higher serum sodium level (P<0.05) compared with group 1. Hyponatremia developed in 6 patients (43%) in group 1 and 0 patients in group 2 (P<0.05). Group 2 also demonstrated a lower urine volume, lower infusion volume (P<0.05) required for hypervolemic therapy, and higher CVP (P<0.05). Failure to maintain CVP was observed in 12 patients (86%) in group 1 and 3 patients (21%) in group 2 (P<0.05). Hydrocortisone caused no serious side effects. Hydrocortisone clearly attenuates excessive natriuresis. Prophylactic hydrocortisone administration appears to have a therapeutic value in inducing hypervolemia efficiently after SAH.
    Stroke 12/2003; 34(12):2807-11. · 6.16 Impact Factor
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    ABSTRACT: Hydrocephalus induces interstitial brain edema, which causes neurological deficits, even if the intracranial pressure is maintained within the normal range, and the cerebral blood flow (CBF) does not decline to an ischemic level. The precise mechanisms underlying such edema-induced neuronal dysfunction remain unclear. In the present study, in an attempt to elucidate the metabolic derangements in brain tissue with interstitial edema, we evaluated the changes in CBF and oxidative/glucose metabolism using a rat model of kaolin-induced hydrocephalus. Hydrocephalus was produced in male Wistar rats by intrathecal injection of 0.1 ml aluminum silicate suspension (200 mg/ml) via the cisterna magna. CBF was determined by 14[C]-iodoantipyrine autoradiography. Oxidative metabolism was evaluated by cytochrome oxidase (CYO) histochemistry, and glucose metabolism by hexokinase (HK) histochemistry. CBF declined with the development of hydrocephalus, but did not reach an ischemic level. The CYO activity was diffusely depressed in both the cortex and hippocampus. The HK activity was preserved at the early stage of hydrocephalus. At the advanced stage, the HK activity was reduced in the hippocampal CA3 region first, and diffusely thereafter. In conclusion, interstitial brain edema impairs oxidative metabolism even at the early stage of hydrocephalus, and shifts the metabolism to anaerobic glycolysis despite a preserved CBF. Impairment of glucose metabolism was first observed in the CA3 region, suggesting that the CA3 is metabolically vulnerable, and CA3 dysfunction may contribute to the memory deficits seen in hydrocephalus.
    Acta neurochirurgica. Supplement 02/2003; 86:545-7.
  • Y Katayama, T Kawamata
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    ABSTRACT: The early massive edema caused by severe cerebral contusion results in progressive intracranial pressure (ICP) elevation and clinical deterioration within 24-72 hours post-trauma. Surgical excision of the necrotic brain tissue represents the only therapy, which can provide satisfactory control of the elevated ICP and clinical deterioration. In order to elucidate the mechanisms underlying the early massive edema, we have carried out a series of detailed clinical studies. Diffusion magnetic resonance (MR) imaging and apparent diffusion co-efficient (ADC) mapping suggest that cells in the central area of contusion undergo shrinkage, disintegration and homogenization, whereas cellular swelling is predominant in the peripheral area during the period of 24-72 hours post-trauma. The ADC values in the central and peripheral areas are maximally dissociated during this period. A large amount of edema fluid accumulates within the necrotic brain tissue of the central area beginning at approximately 24 hours post-trauma. We have found that fluid-blood interface formation within the central area does not represent an uncommon finding in various neuroimaging examinations of cerebral contusions, indicating layering of red blood cells within the necrotic brain tissue accumulating voluminous edema fluid. Intravenous slow infusion of gadolinium-DTPA and delayed MR imaging revealed that the central area of contusion can be enhanced at 24-48 hours post-trauma. implying that water supply from the blood vessels is not completely interrupted. Necrotic brain tissue sampled from the central area of contusion during surgery demonstrates a very high osmolality. It appears that the capacitance for edema fluid accumulation increases in the central area, whereas cellular swelling in the peripheral area elevates the resistance for edema fluid propagation. Combination of these circumstances may facilitate edema fluid accumulation in the central area. We also suggest that the dissociation of ADC values and high osmolality within the necrotic brain tissue may generate an osmotic potential across the central and peripheral areas and contribute to the early massive edema caused by cerebral contusion.
    Acta neurochirurgica. Supplement 02/2003; 86:323-7.

Publication Stats

1k Citations
92.70 Total Impact Points

Institutions

  • 1999–2011
    • Nihon University
      • • Department of Neurological Surgery
      • • Department of Medicine
      Edo, Tōkyō, Japan
  • 1992
    • Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center
      Torrance, California, United States
  • 1991–1992
    • University of California, Los Angeles
      • Department of Neurosurgery
      Los Angeles, California, United States