Shinya Yoshinaga

Cerebral blood flow and autoregulation in normal pressure hydrocephalus.

OBJECTIVE We tried to identify indications for cerebrospinal fluid shunting in patients with normal pressure hydrocephalus. METHODS We studied the cerebral blood flow (CBF) and vascular response to acetazolamide in the white matter, cortex, and thalamus of 21 patients with normal pressure hydrocephalus, comparing patients who improved clinically after shunting with those who did not. We used xenon-enhanced computed tomography for the CBF measurements. RESULTS Preoperatively, both groups had globally reduced CBF, but the reduction was more pronounced in the unimproved patients. The vascular response was impaired only in the white matter of the patients who improved later. After shunting, restoration of CBF, more marked in the white matter, and recovery of vascular response in the white matter paralleled clinical improvement and a reduction in ventricular dilation and periventricular lucency on computed tomographic scans in nine patients. The CBF reduction, however, deteriorated in the 12 patients who did not improve clinically. CONCLUSION We conclude that the underlying disease in the improved patients was ischemia, with a loss of autoregulatory capacity in the periventricular white matter caused by cerebrospinal fluid diffusion. Those who did not improve had irreversible brain damage in which the CBF reduction was secondary to metabolic depression and autoregulation was preserved. We also conclude that patients suspected of having normal pressure hydrocephalus will improve clinically after shunting if preoperative hemispheric CBF is greater than 20 ml/100 g per minute and the vascular response to acetazolamide is impaired only in the periventricular white matter. They will not improve, however, if the preoperative CBF is less than 20 ml/100 g per minute and the vascular response to acetazolamide is intact.

Xenon-enhanced computed tomographic measurement of cerebral blood flow in patients with chronic subdural hematomas.

We compared clinical symptoms with extent of brain shift on computed tomographic (CT) scans and quantitative and three-dimensional measurements of cerebral blood flow (CBF) on xenon-enhanced CT scans in 10 patients with chronic subdural hematomas. Five patients had only headache and minimal or no brain shift on a CT scan. The other five had hemiparesis and/or mental disturbance in addition to headache and moderate or severe brain shift on a CT scan. The mean hemispheric CBF decreased about 7% in patients with headache and about 35% in patients with hemiparesis and/or mental disturbance. It decreased also on the side without the hematoma. The CBF reduction was always more pronounced in the putamen and thalamus than in the cortex. On the contrary, the cortex CBF was mostly preserved or even elevated in both groups of patients. We speculate that CBF reduction in patients with a chronic subdural hematoma occurs initially in central cerebral areas like the basal ganglia and thalamus, and then extends to the entire hemisphere including the cortex as brain compression and displacement progress. Central cerebral area involvement might be more responsible for clinical symptoms than the cortex.

Cerebral blood flow and intracranial pressure in chronic subdural hematomas

BACKGROUND We examined the cerebral blood flow (CBF) and intracranial pressure (ICP) in 15 patients with chronic subdural hematomas to clarify the clinical pathophysiology of this disorder. METHODS All patients had hemiparesis and/or mental disturbance, including confusion or lethargy, and demonstrated either midline shift or herniation on computed tomography (CT) scans. CBF was measured using xenon-enhanced CT preoperatively, 1 day postoperatively, and 3-4 weeks later. ICP was monitored continuously for 24 hours both before and after surgery. RESULTS The CBF was severely reduced on both sides. It stayed at the preoperative level 1 day after surgery, when all patients improved clinically, but returned to subnormal levels in 3-4 weeks. Acetazolamide-enhanced CBF values that were abnormally elevated in each region preoperatively stayed the same during each stage in the hemisphere and cortex despite the different baseline values. However, these measurements increased gradually after surgery in the thalamus and putamen. The ICP was moderately high preoperatively (14.2-25.3 mmHg; mean: 19.4 +/- 3.7 mmHg) and remained high (13.4-31.7 mmHg; mean: 21.4 +/- 6.0 mmHg) 1 day postoperatively. There was no correlation between the CBF values and ICP values in any region either before surgery or 1 day after surgery. CONCLUSIONS We conclude that chronic subdural hematomas may induce neurologic dysfunction primarily through a mechanical distortion of central brain regions such as the thalamus with a secondary influence on remote regions due to transneural depression. The effect of a subdural hematoma on CBF and ICP is not a major cause of neurologic dysfunction. The thalamus seems to be at the core of the pathophysiology of chronic subdural hematomas.

Computed tomography and cerebral blood flow correlations of mental changes in chronic subdural hematoma.

To elucidate the pathophysiology of mental disturbances associated with chronic subdural hematoma, we performed quantitative and three-dimensional measurements of cerebral blood flow (CBF) on xenon-enhanced computed tomographic scans in 12 patients who had chronic subdural hematomas and manifested mental disturbances. In 2 patients who had no headache or hemiparesis, minimal mass effect, and severe multiple infarctions on computed tomographic scan, mentation did not improve after surgery. The CBF reduction was severe, and it further deteriorated after surgery. On the other hand, mentation improved to a varied extent in the other 10 patients, who had headache and/or hemiparesis and minimal, moderate, or severe mass effect and minimal or moderate multiple infarctions on computed tomographic scan. The CBF reduction was diffuse on both sides, but was more marked in the thalamus and putamen than it was in the cortex and subcortex. It was restored after surgery, but insufficiently. The restoration rate was statistically significant only in the thalamus, on both sides (with and without hematoma) (P less than 0.05). Dementia scores and CBF values after surgery were correlated on the side with the hematoma in the frontal cortex and thalamus (P less than 0.01) and in the hemisphere and temporoparietal cortex (P less than 0.05). There was no correlation on the side with the hematoma in the occipital cortex, putamen, and frontal and temporoparieto-occipital subcortices or on the side without the hematoma. The thalamus undergoes displacement and distortion by the hematoma, which in turn leads to changes in consciousness. Postoperative residual mental deficits consist primarily of dementia related to preexisting multiple infarctions.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcified chronic subdural hematoma with intracerebral rupture forming a subcortical hematoma: A case report

We report a calcified chronic subdural hematoma which ruptured intracerebrally forming an acute subcortical hematoma in the frontal lobe in a 59-year-old woman with long-standing liver cirrhosis. Both hematoma cavities communicated each other through a small defect within the inner membrane of the subdural hematoma. The content of both hematomas was identical and was of a clay-like clot. The inner membrane around this communication consisted of thick, very vascular granulation tissue with many hemosiderin deposits and was tightly adherent to the cortex. We speculated that a fresh bleeding into the granulation tissue resulted in formation of a subcortical hematoma through a rupture of the inner membrane. Disseminated intravascular coagulation likely played an important role in this unusual condition.

Multiple intracerebral arteriovenous malformations: report of two cases.

We report the cases of two patients, each of whom had two separate angiographically demonstrable intracerebral arteriovenous malformations (AVMs). One patient had an intraventricular hemorrhage with AVMs in the basal ganglia and the insula on the left side, and the other had a pontine hemorrhage with AVMs in the pons and the occipital lobe on the right side. The AVMs in the former patient were removed totally without residual neurological deficit. We discuss the diagnostic problems of multiple intracerebral AVMs and stress the need for thorough neuroradiological evaluation so as not to miss an occult AVM. We also stress the necessity of total excision of all the lesions and point out several problems faced in surgery for AVMs.

Elevation of the Petrous Bone Caused by Hyperplasia of the Occipital Bone Presenting as Hemifacial Spasm: Diagnostic Values of Magnetic Resonance Imaging and Three-Dimensional Computed Tomographic Images in a Bone Anomaly

A case of elevation of the petrous bone due to hyperplasia of the occipital bone presenting as hemifacial spasm is reported. A 44-year-old man sought treatment for twitching of the buccal muscles on the right side that progressed rapidly in severity within 2 weeks of the onset. The anatomical details of the petrous and occipital bones were delineated clearly by computed tomographic scans of a bone window level. Details of the brain stem were shown by magnetic resonance images. The bone anomaly was displayed more realistically by three-dimensional computed tomographic reconstructions. The faithful representation of structures with these radiological studies should be mandatory, to prepare the surgical planning of such a complicated bone anomaly.

Scalp cavernous angioma presenting as sinus pericranii: diagnostic value of cerebral angiography and magnetic resonance imaging.

Abstract  Objects: Sinus pericranii is only a symptom complex, and it can have a variety of etiologies. Therefore, it is important to differentiate these etiologies preoperatively by means of radiological examinations. A 5-year-old boy was admitted with a soft and fluctuant tumor in the right parietal region near the midline. The tumor appeared when the child was in a recumbent position, distending noticeably with the Valsalva maneuver and disappearing completely when the patient was in the sitting position. Methods: Magnetic resonance imaging showed the lesion with honeycomb-like heterogeneous iso- and low-intensity signals on the T1-weighted image and with heterogeneous high- and iso- intensity signal on the T2-weighted image. Dynamic study with an injection of gadolinium diethylene-triaminopentaacetic acid demonstrated and nodular peripheral enhancement at early phase and subsequent progressive enhancement towards the center of tumor. The internal carotid angiogram was normal. The external carotid angiogram, however, showed a tumor stain fed by the superficial temporal arteries. The stain was retained until the late phase and drained into the scalp veins and into the superior sagittal sinus. Following direct injection of contrast medium into the tumor there was prolonged retention of the medium in the tumor and leakage into scalp veins and the superior sagittal sinus. The mass under the periosteum was totally removed and proved to be a cavernous angioma. Conclusions: Scalp cavernous angioma is one of the etiologies of sinus pericranii and may be diagnosed preoperatively by cerebral angiography or magnetic resonance imaging. Serial dynamic magnetic resonance imaging will be particularly helpful for this diagnosis.

Postoperative subarachnoid clots and the pattern of cerebral ischemia associated with symptomatic vasospasm.

OBJECTIVE We retrospectively evaluated the presence of subarachnoid clots and the development of symptomatic vasospasm in 125 patients who had early surgical treatment of a ruptured cerebral aneurysm. SUBJECTS AND METHODS We studied 16 patients (aged 35-86 years; mean, 58.7 years) who underwent surgery 0 to 6 days (mean, 2.1 days) and then manifested symptomatic vasospasm on day 5-12 (mean, day 7.4), and 57 patients (aged 13-79 years; mean, 52.0 years) who underwent surgery 0-8 (mean, day 2.9) and did not manifest symptomatic vasospasm. The volume and location of subarachnoid clots were evaluated with computed tomographic (CT) scanning. Cerebral ischemia was evaluated clinically and also in eight patients, by measurement of cerebral blood flow (CBF) using xenon-enhanced CT. Angiographic evaluation was performed only on one patient. RESULTS Of the 16 patients with symptomatic vasospasm, the subarachnoid clots were localized, distributed thickly, or associated with intracerebral hematomas in 15 and thin in 1 at the time of admission. Fifteen patients had CT evidence of a subarachnoid clot during vasospasm. Most of the clots were near the ruptured aneurysms, but in three cases, clots were located in the remote cisterns, which were not accessible operatively. The clinical manifestations of vasospasm in these three patients correlated with the site of the clot. CBF was reduced in the territory of the involved artery in all eight patients in whom it was measured. In two of the eight cases, the reduction occurred in the territory of a contralateral artery. In contrast, in the 57 patients without symptomatic vasospasm, the subarachnoid clots were already gone or disappeared soon after surgery in most patients. CONCLUSIONS The continued presence of subarachnoid clots is an important risk factor for symptomatic vasospasm after the rupture of a cerebral aneurysm. The clot is not always located near the ruptured aneurysm, and the clinical course may be unpredictable.

Hyponatremia-induced metabolic encephalopathy caused by Rathke's cleft cyst: a case report.

Rathkes cleft cysts are sometimes associated with aseptic meningitis or metabolic encephalopathy due to hyponatremia. We treated such a case manifest by lethargy, fever and electroencephalographic abnormalities. A 68-year-old man was admitted to our ward after experiencing general malaise, nausea and vomiting and then high fever and lethargy. On admission, he was drowsy and had nuchal rigidity and Kernigs sign. Physically, he was pale with dry, thickened skin. He had lost 5.0 kg of body weight in the last month. His serum sodium was 115 mEq/l. He had a low serum osmotic pressure (235 mOsmol/l) and a high urine osmotic pressure (520 mOsmol/l). His urine volume was 1200-1900 ml/24 h with a specific gravity of 1008-1015. The urine sodium was 210 mEq/l. He did not have an elevated level of antidiuretic hormone. Electroencephalograms showed periodic delta waves over a background of theta waves. With sodium replacement, the patient become alert and symptom free, and his electroencephalographic findings normalized. However, the serum sodium level did not stabilize, sometimes falling with a recurrence of symptoms. Magnetic resonance imaging clearly delineated a dumbbell-shaped intrasellar and suprasellar cyst. The suprasellar component subsequently shrunk spontaneously and finally disappeared. An endocrinologic evaluation showed panhypopituitarism. The patient was given glucocorticoid and thyroxine replacement therapy, which stabilized his serum sodium level and permanently relieved his symptoms. A transsphenoidal approach was performed. A greenish cyst was punctured, and a yellow fluid was aspirated. The cyst proved to be simple or cubic stratified epithelium, and a diagnosis of Rathkes cleft cyst was made. The patient was discharged in good condition with a continuation of hormonal therapy. Rathkes cleft cyst can cause aseptic meningitis if the cyst ruptures and its contents spill into the subarachnoid space. Metabolic encephalopathy induced by hyponatremia due to salt wasting also can occur if the lesion injures the hypothalamus and pituitary gland.