Intracerebral hemorrhage secondary to vitamin K deficiency is presented in three newborn infants: 4 days, 28 days and 21 days of age respectively. After the administration of vitamin K(5-10 mg) either intravenously or intramusculary, prolonged prothrombin time(PT) and partial thromboplastin time(PTT) were corrected promptly. Vitamin K dependent coagulation factor deficiency due to vitamin K deficiency is accounted for the pathogenesis of hemorrhage. The possible causes of vitamin K deficiency, diagnostic methods and treatment of this disease entity are reviewed. Neurosurgeons as well as pediatricians should remain alert for the development of intracerebral hemorrhage caused by vitamin K deficiency in neonatal period.
Blood Coagulation Factors ; Cerebral Hemorrhage* ; Hemorrhage ; Humans ; Infant, Newborn* ; Partial Thromboplastin Time ; Prothrombin ; Prothrombin Time ; Thromboplastin ; Vitamin K Deficiency* ; Vitamin K* ; Vitamins*

The effect of nicardipine was investigated on hypertension due to raised intracranial pressure, pressor response of alpha-adrenoceptor agonists in the dissected thoracic aorta. Intracerebroventricular(icv) and intravenous(iv) nicardipine produced dose-dependent depressor response and bradycardiac effect, especially marked response was observed following iv injection. The pressor response to raised intracranial pressures was potentiated following iv injection of 50 microgram/kg nicardipine but was markedly inhibited following iv 100 microgram/kg injection, and was not affected following icv 50 microgram/kg administration but was markedly inhibited following icv administration of 100-200 microgram/kg nicardipine. The nicardipine inhibited contractile effect of KCI 35 mM in a dose-dependent fashion but did not affect that of Ne and ME. These data suggest that nicardipine caused hypotensive effect by blocking calcium influx in the peripheral vessels and that direct effect of nicardipine on central nervous system involves the hypotensive action. Conclusively, the inhibitory effect of nicardipine on the pressor response to the intracranial pressure elevation may be induced by these two mechanisms.
Aorta, Thoracic ; Calcium ; Central Nervous System ; Hypertension ; Intracranial Pressure* ; Nicardipine*

This study was undertaken to observe the effects of centrally administred antihistamines on the blood pressure. Diphenhydramine(DPH), a H1-receptor antagonist, and ranitidine(RAN), a H2-receptor antagonist were administered intracerebroventricularly(icv) on urethane-anesthetized rabbits. 1) Both DPH and RAN administered intraccebroventricularly increased blood pressure, however the intravenous(iv) adminstration of them did not affect blood pressure. The pressor response to icv DPH was dose-dependent, but that to icv RAN was not. 2) The pressor response to icv DPH(1mg) was either markedly attenuated or reversed to depressor response by the pretreatment with icv phentolamine(250,500ug), and iv chlorisondamine(0.1, 1mg/Kg) and iv phenoxybenzamine(1mg/Kg). In cord-sectioned rabbtis, icv RAN) 1mg) did not produce pressor response. 3) The pressor responsr to icv RAN(1mg) was not affected by the pretreatment with icv phentolamine(500ug), iv chlorisondamin(1mg/Kg) and iv phenoxybenzamine(1mg/Kg), and iv phenoxybenzamine(1mg/Kg). RAN also producted pressor response in cordsectioned rabbits. These results suggest that the pressor response to icv DPH is elecited by increasing peripheral sympathetic tone via the stimulation of central alpha-adrenoreceptors and the pressor response to icv RAN is produced by releasing some humoral facotr which can increase blood pressure.
Blood Pressure ; Diphenhydramine* ; Histamine Antagonists ; Rabbits* ; Ranitidine*

Effect of infusion and bolus injection of lidocaine on the pressure response to the increased intracranial pressure(ICP) was investigated in urethane-anesthetized rabbits. 1) Arterial blood pressure(BP) and ICP were significantly raised by infusing saline(0.05ml/min) into an epidural balloon. 2) Infusing of lidocaine(0.5mg/kg/min) into an ear vein minutely inhibited the elevation of BP and ICP when infusing saline into an epidural balloon. However, infusion of lidocaine(1.5mg/kg/min) markedly inhibited the elevation of BP and ICP. 3) Repeating the infusion of saline into the epidural balloon with intervals, the duration reached to the level of 80-10 mmHg ICP was gradually shortened. Each depressor response to the first, second and third injection of lidocaine(3 mg/kg) was similar. The first injection transiently reduced the elevated ICP, but the second and third injection reduced that significantly and the reducing effect was gradually prolonged according to repeating the lidocaine injection. These results show that lidocaine could delay the elevation of ICP and reduce the previously increased ICP by infusing saline into an epidural balloon.
Ear ; Intracranial Hypertension* ; Lidocaine* ; Rabbits* ; Veins

A K+-channel blocker, 4-aminopyridine(4-AP) increases neurotransmitter release from motor nerve terminals and has been shown to restore neuromuscular transmission in the myasthenic syndrome. It has been reported that the intravenous injection of 4-AP in the myasthenic patients caused many central adverse effects including anxiety and restlessness, but did not affect the blood pressure. The aim of this study was to observe the effect of intracerebroventricularly administered 4-AP on the blood pressure and to elucidate the mechanism of the action in urethane-anesthetized rabbits. Intracerebroventricular(icv) 4-AP produced pressor effects in a dose-dependent fashion, but intravenous(iv) 4-AP of the same dose did not altered the blood pressure. Tetraethylammonium, a K+-channel blocker which differs from 4-AP structurally, had little effect on the blood pressure, but 3,4-diaminopyridine, another derivative of the aminopyridine, produced pressor effect similar to 4-AP. The pressor effect of icv 4-AP was not affected by the treatment with iv phenoxybenzamine and chlorisondamine, and in bilateral adrenalectomized rabbits. These results suggest that the 4-AP pressor effect is not related to the periphral sympathetic nerve nor adrenal gland. The pretreatment with icv phentolamine and prazosin did not altered the 4-AP pressor. However, the icv 4-AP pressor effect was significantly attenuated by the treatment with icv yohimbine, and significantly potentiated by the treatment with icv clonidine. The treatment with icv diltiazem markedly inhibited the icv 4-AP pressor effect. It is concluded that 4-AP-sensitive K+-channels in rabbit brain might play a role in the regulation of blood pressure and that the 4-AP pressor effect is closely related to the central alpha2-adrenoceptors and L-type calcium channels.
4-Aminopyridine* ; Adrenal Glands ; Anxiety ; Arterial Pressure* ; Blood Pressure ; Brain ; Calcium Channels, L-Type ; Chlorisondamine ; Clonidine ; Diltiazem ; Humans ; Injections, Intravenous ; Neurotransmitter Agents ; Phenoxybenzamine ; Phentolamine ; Prazosin ; Psychomotor Agitation ; Rabbits ; Tetraethylammonium ; Yohimbine

The authors describe three patients of syringomyelia associated with posterior fossa tumor. The lesions were diagnosed by magnetic resonance imaging. Total removal of tumor without decompression of foramen magnum was done and regression of syringomyelia and improvement of symptoms were demonstrated. It is suggested that the blockage of cerebrospinal fluid flow at the foramen magnum by tonsilar herniation may play an important role in syrinx formation.
Cerebrospinal Fluid ; Decompression ; Foramen Magnum ; Humans ; Infratentorial Neoplasms* ; Magnetic Resonance Imaging ; Syringomyelia*

A case of intradural spinal lipoma without congenital abnormalities is presented. A 37 year-old male was admitted to our hospital because of paralysis of both legs and sphincteric disturbance. Neurologic findings were spastic paraplegia, hypesthesia on the level of T10, 11 dermatoma, anesthesia below the level of T12 dermatoma, Beevor's sign, bilateral ankle clonus and Babinski sign. Plain thoracolumbar spine X-ray showed widening of the interpedicular distances of T10, 11 in A-P view, and scalloping in the posterior aspect of the bodies of T10, 11 in lateral view. Myelogram showed widening of the dye column and double cup-like filling defect at the level of the T12 spinal body. Total laminectomy was performed from L1 through T9. The tumor located from T10 to T12 of the spinal level intradurally, and also diffusely infiltrated the cord, making complete removal impossible. The histopathologic examination confirmed the lipoma. The patient was discharged without improvement of neurologic deficits.
Adult ; Anesthesia ; Ankle ; Congenital Abnormalities ; Humans ; Hypesthesia ; Laminectomy ; Leg ; Lipoma* ; Male ; Neurologic Manifestations ; Paralysis ; Paraplegia ; Pectinidae ; Reflex, Babinski ; Spinal Cord* ; Spine

Hearing loss in the contralateral functioning ear is a rare and distressing complication after vetibular schwannoma removal. Various possible mechanisms have been proposed, however, the etiology of hearing loss is not clear. Fortunately, this is an extremely rare occurrence, sporadic case reports have appeared in the literatures. We report two cases of acute contralateral hearing loss after vestibular schwannoma removal and discuss the possible mechanisms of the phenomenon. Although permanent deafness may result, in our cases, the hearing loss was temporary, returning to near preoperative level within one month. The etiology of hearing loss in one case is thought to be cerebrospinal fluid leakage. However, in the other case, the cause of hearing loss is not clear. A better understanding of these events may lead to preventive measures to avoid contralateral hearing loss after vestibular schwannoma removal.
Cerebrospinal Fluid ; Deafness ; Ear* ; Hearing Loss* ; Hearing* ; Neurilemmoma ; Neuroma, Acoustic*

Effects of a M1 receptor antagonist, pirenzepine, a M2 receptor antagonist, AF-DX116, and a nicotinic receptor antagonist, mecamylamine on the pressor responses to preganglionic sympathetic nerve stimulation(PNS) and McN-A-343 and DMPP in spinal(pithed) rabbits were investigated in order to elucidate a functional role of M1, M2 and nicotinic receptors in ganglionic transmission. Pirenzepine and AF-DX116 selectively inhibited the McN-A-343-induced pressor reponse in chlorisondamine-treated rabbit and the BCh-induced bradycardia, respectively. Electrical stimulations of preganglionic sympathetic outflow at T8 level produced increases in blood pressure. Pirenzepine(3 microgram/kg) significantly inhibited the PNS-induced pressor response and the degree of inhibition was not changed by increasing the doses to 100 microgram/kg. AF-DX116(100 microgram/kg) had no effect on the PNS-induced pressor response. Mecamylamine inhibited the PNS-induced pressor response in a dose-dependent manner. The inhibitory action of mecamylamine was significantly augmented by combined-treatment with pirenzepine(30 microgram/kg) but AF-DX116(100 microgram/kg) did not affect the inhibitory action of mecamylamine. McN-A-343 and DMPP elicited pressor response in the spinal rabbit. Pirenzepine and AF-DX116 dose-dependently inhibited the McN-A-343-induced pressor response but they did not affect DMPP-induced pressor response. Mecamylamine inhibited both pressor responses induced by Mc-N-343- and DMPP. These results suggest that not only nicotinic receptors but also M1 receptors play a facilitatory role in ganglionic transmission but M2 receptors do not contribute the transmission in spinal(pithed) rabbits.
(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium Chloride ; Blood Pressure ; Bradycardia ; Dimethylphenylpiperazinium Iodide ; Electric Stimulation ; Ganglia, Sympathetic* ; Ganglion Cysts ; Mecamylamine ; Pirenzepine ; Rabbits ; Receptors, Nicotinic*

No abstract available.
Vulva* ; Vulvar Neoplasms*