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

Rathke's 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 Kernig's 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 Rathke's cleft cyst was made. The patient was discharged in good condition with a continuation of hormonal therapy. Rathke's 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.

Cerebral blood flow and clinical outcome in patients with thalamic hemorrhages: a comparison with putaminal hemorrhages.

It has been reported that the reduction of cerebral blood flow (CBF) is more pronounced with thalamic hemorrhages than with putaminal hemorrhages, and the clinical outcome is worse with the former. However, the mechanism underlying these differences is not clear. We compared neurologic status, hematoma volumes, outcome scores. and early (< 1 month) and late (2-12 month) CBF values between 15 patients with thalamic hemorrhages and 28 patients with putaminal hemorrhages. We also correlated thalamic versus hemispheric CBF on each side and ipsilateral versus contralateral thalamic and hemispheric CBF. Finally, we evaluated the response to acetazolamide during the late stage. Thalamic hemorrhages were associated with a more pronounced reduction in CBF bilaterally, even though their hematoma volumes were much smaller. Contralateral to the hemorrhage, the discrepancy in CBF values between the two groups became greater in the late stage because CBF started to recover in putaminal hemorrhages but persistently deteriorated in thalamic hemorrhages. In the group with thalamic hemorrhages, the correlation between thalamic and hemispheric CBF ipsilateral to the hemorrhage and between thalamic CBF on both sides was disrupted in the early stage and restored in the late stage, whereas the correlation between the hemispheric CBF values was consistently preserved. Acetazolamide invariably augumented CBF during the late stage. The clinical outcome was worse in the thalamic group, but CBF values correlated negatively with outcome in both groups. We conclude that the reduction of CBF in the late stage may be secondary to metabolic depression due to transneural depression ('diaschisis'). The metabolic depression in thalamic hemorrhages is more extensive and persistent than in putaminal hemorrhages, which probably accounts for both the more pronounced CBF reduction and the worse outcome.

Cerebral blood flow in normal brain tissue of patients with intracranial tumors.

Pre- and postoperative cerebral blood flow (CBF) changes in the normal brain tissue of 17 patients with intracranial tumors were studied to determine the value for planning therapeutic strategy. The tumors included eight astrocytomas, seven meningiomas, one metastasis, and one arachnoid cyst. The patients were divided into two groups based on the mass effect seen on computed tomography (CT) scans. Group A comprised six patients with midline shift or evidence of herniation; Group B, 11 patients with no mass effect or local compression only. CBF and vasoresponse to acetazolamide were measured in the bilateral hemispheres, cortices, and thalami using xenon-enhanced CT, excluding the area of tumor extension, before and 2-3 weeks after tumor excision. Preoperative CBF was reduced bilaterally but more markedly ipsilateral to the tumor. The CBF reduction was significantly greater in Group A than in Group B. Acetazolamide caused CBF to increase by 70.5-99.1% in Group B but only increase by 1.7-9.6% or paradoxically decrease in Group A. Postoperatively, the CBF tended to recover partially in Group A but persisted or deteriorated in Group B. The more pronounced CBF reduction and poor or paradoxical response to acetazolamide preoperatively and postoperative CBF restoration in Group A may indicate that ischemia was more important than metabolic depression in these patients. In contrast, the excessive response to acetazolamide and the postoperative CBF deterioration in Group B may indicate that CBF reduction was secondary to metabolic depression. Mass effect is a key predictor for functional recovery following surgical decompression of intracranial tumors.

Significance of periventricular hemodynamics in normal pressure hydrocephalus.

To delineate the pathophysiology of periventricular hemodynamics in normal pressure hydrocephalus, we performed quantitative and three-dimensional measurements of cerebral blood flow (CBF) by using xenon-enhanced computed tomographic scans. Measurements were made on 7 patients in whom normal pressure hydrocephalus after subarachnoid hemorrhage had been confirmed by clinical improvement after shunting. We compared mean CBF values in the white matter and cortex of the frontal, temporal, parietal, and occipital lobes and in the thalamus before and after shunting, with an evaluation of dementia and the extent of ventricular dilation and periventricular lucency on computed tomographic scans. CBF returned to within normal limits in the white matter of the frontal and temporoparieto-occipital lobes. CBF restoration closely correlated with clinical improvement and reduction in ventricular dilation and periventricular lucency. We speculate that ischemia occurs initially in the periventricular white matter as a result of diffused cerebrospinal fluid and then extends of the cortex and to the thalamus, causing a "misery perfusion" state with neuronal dysfunction. Incomplete improvement of dementia and CBF in the cortex and thalamus may be explained by preexisting arteriosclerosis in aged patients, coexisting brain damage caused by subarachnoid hemorrhage and subsequent surgical insult in aneurysm patients, and delayed recovery of cortical function that has been secondarily impaired by the periventricular lesions.