No abstract available.
Chlamydia* ; Fluorescent Antibody Technique, Indirect*

The intracranial arachnoid cyst is distinctly uncommon and they have unusual clinical course. The plain skull series were usually shown bulging of the overlying skull due to progressive collection of cerebrospinal fluid in cystic cavity. Pre-operative diagnosis is unlikely to be made. The predilection sites of this lesion are usually convexity of hemisphere, cisterna chiasmaticus, especiaily forebrain along the axis of main cerebral artery. The authors report a case of intracranial arachnoid cyst arisen along the Sylvian fissure combined chronic subdural hematoma follwoing sustained mild head injury. The pathologic diagnosis was arachnoid cyst, since the removed cyst wall was normal arachnoid tissue.
Arachnoid ; Arachnoid Cysts* ; Axis, Cervical Vertebra ; Cerebral Arteries ; Cerebrospinal Fluid ; Craniocerebral Trauma ; Diagnosis ; Hematoma, Subdural, Chronic ; Prosencephalon ; Skull

Spontaneous cerebellar hemorrhage is classically considered a rare and fatal disease because the early diagnosis is very rarely made during the life, and there is scant mention of the problems of spontaneous hemorrhage into the cerebellar hemisphere. However our opinions indicate that its frequency is greater than is generally thought although it is considered a rare lesion. The purpose of this paper is to record our present opinions concerning the possible early diagnosis and surgical management of the spontaneous cerebellar hemorrhage. We believe that it is possible by clinical examination alone to make or strongly suspect the diagnosis in life during the early stage before irreversible damage occurs and that emergency surgical intervention is strongly indicated. The patients is a 38 year old man admitted to the Department of Neurosurgery, Catholic Medical Center on Nov 3, 1976 with severe headache, vomiting, dysarthria and mental confusion. On examination, he was disclosed mental confusion, repeated vomiting, constricred pupil, horizontal nystagmus, inability to stand, dysarthria and neck stiffness. We confirmed the diagnosis under the cerebellar hemorrhage involving the cerebellar vermis and both cerebellar hemispheres by means of vertebral and carotid angiography, conray ventriculography, and cerebrospinal fluid examination. We underwent suboccipital craniectomy with the evacuation of hematoma at the vermis and both cerebellar hemispheres after 48 hours of onset of illness and his postoperative course was good except for mild cerebellar dysfunction signs and he was discharged on 45th hospital days.
Adult ; Angiography ; Cerebellar Diseases ; Cerebrospinal Fluid ; Diagnosis ; Dysarthria ; Early Diagnosis ; Emergencies ; Headache ; Hematoma ; Hemorrhage* ; Humans ; Neck ; Neurosurgery ; Nystagmus, Pathologic ; Pupil ; Vomiting

No abstract available.
Aneurysm ; Aneurysm, Ruptured* ; Cerebral Veins* ; Veins*

One hundred eighty infants with oxygen therapy who were under 2,500gm birth weight or under 37 weeks of gestational age, were examined between January 1990 and November 1992. We performed clnical analysis and results were as follows. 1) Fifty six infants (31.1%) were diagnosed as retinopathy of prematurity. 2) The first examination was performed at 2.5 weeks of life on average, and the retinopathy of prematurity was diagnosed at 3.8 weeks on average. 3) The incidence of retinopathy of prematurity was highly associated with low birth weight (< or =1,890 gm), low gestational age ( < or =33.1 weeks), and high oxygen concentration with long duration (FiO2> or =0.4 over 1 week)(P<0.005). 4) Other associated risk factors were idiopathic respiratory distress syndrome, anemia, neonatal hypoxia and sepsis.
Anemia, Neonatal ; Anoxia ; Birth Weight ; Gestational Age ; Humans ; Incidence ; Infant ; Infant, Low Birth Weight ; Infant, Newborn ; Oxygen ; Retinopathy of Prematurity* ; Risk Factors ; Sepsis

No abstract available.
Female ; Pregnancy ; Pregnancy, Ectopic*

Attention has been called to the sudden expansion of a pituitary tumor by hemorrhage within it, causing sudden loss of vision. Management of the pituitary apoplexy should be regarded as a neurological emergency. The outstanding clinical features of acute pituitary apoplexy were sudden headache, depressed consciousness, opthalmoplegia, meningismus and signs of compression of the optic nerve or chiasm. The authors report two cases of pituitary apoplexy, one was chromophobe adenoma and pathological diagnosis was not obtained in the other. The first case was 45-year-old man admitted to the Department of Neurosurgery, Catholic Medical Center on June 20, 1977, with headache, double vision and impared left side visual acuity. On April 26, 1977, he experienced sudden severe headache and diplopia then became drowsy. The headache and impairment of consciousness improved subsequently. He was admitted to a university hospital following the onset. The work up at the hospital revealed an enlarged sella with hazy dorsum sellae on plain skull films. The carotid angiogram revealed an elevation of the A1 segments bilaterally and cisternal pneumogram revealed an evidence of suprasellar extension of the pituitary tumor. He was advised to have immediate surgery. The patient, however, refused the surgery and noticed the impaired visual acuity and diplopia were persisting. The studies in this hospital revealed marked impairment of left side vision and oculomotor nerve palsy of the left eye. The carotid angiogram and cisternal pneumogram revealed the no evidence of sellar mass or suprasellar extension of the tumor. The second case was 59-year-old woman admitted to the neurosurgical ward on September 30, 1977, after a sudden onset of severe bifrontal headache, vomiting, bilateral ocular pain and drowsy mental state. She was drowsy with panopthalmoplegia of the right side, and spinal fluid was xanthochromic. Skull X-ray, carotid angiogram and air study revealed an evidence of pituitary tumor with minimal suprasellar extension. Removal of pituitary tumor through the trans-sphenoidal approach was performed, and the tumor was proved to be chromophobe adenoma. Panopthalmoplegia was progressively improved postoperatively.
Adenoma, Chromophobe ; Consciousness ; Diagnosis ; Diplopia ; Emergencies ; Female ; Headache ; Hemorrhage ; Humans ; Meningism ; Middle Aged ; Neurosurgery ; Oculomotor Nerve Diseases ; Optic Nerve ; Pituitary Apoplexy* ; Pituitary Neoplasms ; Skull ; Visual Acuity ; Vomiting

Focal cerebral ischemia was made in 20 adult cats by transorbital middle cerebral artery occlusion (MCAO) under pentobarbital anesthesia. Arterial blood gas, systemic arterial blood pressure (SABP), intracranial pressure (ICP), and regional cerebral blood flow (rCBF) on ectosylvian, suprasylvian, and marginal gyrus of the left hemisphere by hydrogen clearance were measured for 30 minutes before and 120 minutes after middle cerebral artery occlusion. Ten animals were treated with 20 mg/kg of pentoxifylline (PTF) and ten animals with 1ml/kg of normal saline as the control group for 30 minutes before and 30 minutes after middle cerebral artery occlusion. There was no beneficial effect of pentoxifylline (Trental(R)) on basal blood flow over left hemisphere before middle cerebral artery occlusion. Regional cerebral blood flow was highly significantly improved on the marginal gyrus (MG) for 90 minutes after middle cerebral artery occlusion, more remarkable for initial 60 minutes (P<0.01), and also significantly restored on suprasylvian gyrus (SSG) for initial 60 minutes by pentoxifylline (P<0.05). However, pentoxifylline failed to improve regional cerebral flow on extosylvian gyrus (ESG) which was considered dense core of infarct area due to middle cerebral artery occlusion in cat. In addition, pentoxifylline had significant hypotensive effect during intravenous administration for 60 minutes (P<0.05). These findings suggest the possibility of pentoxifylline to ameliorate hemorheological property rather than vasodilating effect in the collaterally perfused area around dense infarct.
Administration, Intravenous ; Adult ; Anesthesia ; Animals ; Arterial Pressure ; Brain Ischemia ; Cats ; Cerebral Infarction* ; Hemorheology ; Humans ; Hydrogen ; Infarction, Middle Cerebral Artery ; Intracranial Pressure ; Pentobarbital ; Pentoxifylline*

No abstract available.
Goldenhar Syndrome*

Excessive activation of the N-methy-D-aspartate(NMDA) subtype of glutamate receptor, has been implicated in the sequence of neurochemical events which results in irreversible neuronal damage in cerebral ischemia. The effect of the NMDA antagonist upon the amount of ischemic brain damage has been already assessed by some investigators. But most of them were performed only in acute ischemic models. In the light of clinical experiences, it's neuroprotective effect is much more important in the prolonged ischemic model. So, authors produced the permanent occlusion of the left middle cerebral artery(MCAO) and sacrificed the animals 48 hours after the occlusion to observe the neuroprotective effect of the NMDA antagonist, MK-801, in the maturated condition of ischemia according to the previous PART I experiment. MK-801 was administered 2 times, intravenously 1 hours prior to MCA occlusion(0.5 mg/kg) and intraperitoneally 1 hour after the induction of ischemia(5 mg/kg) to maintain proper concentration of the drug. CBF was measured by hydrogen clearance methods. Areas of brain infarction were delineated by tetrazolium salt at the preselected 8 coronal levels of forebrain and measured on scale diagrams by a plannimeter. MK-801 had no effect on the cardiopulmonary function. In the control, the basal value of CBF was around 118 ml/100 g/min. Immediately after MCAO, CBF of the ipsilateral cortex was reduced to 13.3+/-2.6 ml/100 g/min and not recovered until the end of the experiment. But CBF of the contralateral cortex was maintained in the basal value throughout the experiment. In the treated, immediately after the intravenous administration of the drug. CBF of both frontal cortices was reduced to 15 to 20% of the basal value(P<0.001), and the reduced CBF was noted even after MCAO, comparing to the control, but 24 hours later the reduced CBF of the contralateral cortex recovered to the basal value. Treatment with MK-801 reduced the total amount of ischemic damage in the cerebral hemisphere(15.82+/-2.41 versus 10.66+/-1.33 cm, P<0.001) and the cerebral cortex(11.0+/-3.73 versus 6.30+/-1.6 cm, P<0.001). But the effect on the caudate nucleus was minimal. This experiment provides evidence for the potency of the glutamate antagonist, MK-801, in reducing ischemic brain damage, despite the result was obtained 48hours after MCAO. And the anti-ischemic effect of MK-801 in the experiment could not be attributed to by improvement of blood flow to the hypoperfused cerebral tissue.
Administration, Intravenous ; Animals ; Brain ; Brain Infarction ; Brain Ischemia ; Caudate Nucleus ; Dizocilpine Maleate* ; Glutamic Acid ; Humans ; Hydrogen ; Infarction, Middle Cerebral Artery* ; Ischemia ; Middle Cerebral Artery* ; N-Methylaspartate* ; Neurons ; Neuroprotective Agents ; Prosencephalon ; Rats* ; Receptors, Glutamate ; Research Personnel