Internal carotid arterial occlusion following mandibular osteotomy.
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Carotid Artery Diseases↗
Biomedical subjects
M J Rosner
Publications and source records attributed to M J Rosner.
Anomalous exit of the C-6 nerve root via the C-6, C-7 foramen.
We report a case of the anomalous exit of the C-6 nerve root at the C-6, C-7 foramen. This caused intense radicular and cervical pain in a 25-year-old woman. At myelography, the 5th and 6th cervical roots appeared conjoined, and at operation the C-6 root and ganglion were found to turn acutely downward, lateral to the pedicle of C-6, and then to exit with the C-7 nerve root through the C-6, C-7 foramen. The ganglion of C-6 was placed nearly parallel to the dural sac and tethered at its origin on the dural sac and at the exit foramen with the C-7 root. The pedicle of C-6 was interposed between the dural sac and the ganglion of C-6. Cervical hemilaminectomy and resection of the pedicle of C-6 defined the anatomy and resulted in a clinical cure. The radiological features are described and contrasted with those of other anomalies. To our knowledge, this is the first report of such an anomalous course of exit of a cervical root.
Adult↗
Constant ventricular drainage: pitfalls and variables. Technical note.
After observing the erratic performance of a commercially available ventricular drainage system, we examined the hydrostatic pressure exerted by the system as a function of the volume of fluid within the drainage bag (at a constant height). Initially, 3 to 4 cm more than the expected 27 cm of height was required to achieve a drainage pressure of 20 mm Hg. As the volume of fluid increased, there was an initial precipitous fall from the 20 mm Hg preset pressure to 14 to 16 mm Hg; this pressure differential increased as the volume of drained fluid increased. Removal of air from the drainage bag resulted in an additional decrement in the observed hydrostatic pressure. These decrements in pressure were not apparent with another commercially available bag used commonly for ventricular drainage. We therefore recommend that, if ventricular drainage is to be accomplished against a constant hydrostatic pressure head, the system should be configured so that the actual hydrostatic pressure against which drainage occurs can be measured quickly and easily. The system should be checked at frequent intervals as the ventricular drainage bag fills. We note additional pitfalls in use of constant ventricular drainage and suggest solutions.
Cerebral Ventricles↗
Origin and evolution of plateau waves. Experimental observations and a theoretical model.
Laboratory observations made in cats with fluid-percussion head injuries have suggested that plateau waves or Lundberg "A-waves" are not independent of systemic circulatory events. Four distinct phases in the evolution of the plateau wave have been identified, and each related to a circulatory change in a causal manner. The first phase is the premonitory drift phase where intracranial pressure (ICP) gradually increases prior to the plateau proper. This phase is caused by a slow gradual decline in systemic arterial blood pressure (SABP) which increases ICP by autoregulatory vasodilation and reduces cerebral perfusion pressure (CPP) to a range of 70 to 80 mm Hg. The second phase is the plateau phase initiated at a CPP of about 70 to 80 mm Hg, and is characterized by a rapid increase in ICP as CPP falls further to 40 to 50 mm Hg. The plateau lasts as long as the CPP remains stable and above ischemic levels. The third phase is the ischemic response, characterized by CPP being returned toward normal by increases in SABP in response to very low CPP's. The fourth phase is the resolution, characterized by a rapid decline in the ICP to baseline levels with stabilization of the SABP and CPP, and is best explained by autoregulatory vasoconstriction. Plateau waves appear to occur as the result of intact or mostly intact autoregulation responding to changes in CPP. The series of events that follow are best explained by what is known of normal autoregulation; the various properties of plateau waves are viewed and explained as the expected and logical consequences of an unstable CPP acting upon a generally intact cerebrovascular bed in the face of elevated ICP and decreased compliance.
Animals↗
Experimental brain injury: successful therapy with the weak base, tromethamine. With an overview of CNS acidosis.
The presence of lactic acidosis in the cerebrospinal fluid of patients suffering brain injury as the result of trauma, subarachnoid hemorrhage, neoplasia, or ischemia has been well documented. The authors theorized that this acidosis becomes harmful in itself, and that treatment with an alkalinizing agent (tris(hydroxymethyl)aminomethane: tromethamine) capable of penetrating the blood-brain barrier would be efficacious. Fifteen pairs of mongrel cats were subjected to a 2.85-atmosphere fluid-percussion injury (LD80), and were supported by respirators for up to 72 hours prior to being placed in cages for an additional 4 days of observation. Experimental cats underwent continuous infusion of tromethamine (begun 10 minutes after injury); control animals were infused with an equal volume of lactated Ringer's solution. Twenty percent of the control group survived until sacrificed on Day 7 post-injury. Survival in the tromethamine group was 60% (p less than 0.05), and morbidity also appeared to be reduced in the treated cats. Intracranial pressure (ICP) in treated cats was 60% (p less than 0.05) of that in the control cats after respirator support for 3 days. Tromethamine infusion was associated with improved survival, decreased morbidity, and decreased ICP when compared with results in control animals. The literature with regard to central nervous system acidosis has been reviewed in an attempt to clarify and define this problem.
Acidosis↗
Mechanical brain injury: the sympathoadrenal response.
Catecholamine release was studied in cats as a function of injury severity in the fluid-percussion model of brain injury. Hyperglycemia was also studied as a function of catecholamine response and injury severity. Epinephrine (E) and norepinephrine (NE) increased as a function of injury. This increase was maximal at about a 3.0-atmosphere (atm) injury level and amounted to a 500-fold increase for E and 100-fold increase for NE. Both catecholamines increased maximally by 10 seconds postinjury. Glucose increased to about 350% of baseline at 500 seconds postinjury and also increased as a function of injury severity. Results suggested that the sympathoadrenal discharge was capable of a graded response which was maximal at about 3.0 atm. Associated with this increase were hypertensin, bradyarrhythmias, tachyarrhythmias, and hyperglycemia.
Adrenal Glands↗
Brain metabolism during increased intracranial pressure as assessed by niroscopy.
Intracranial pressure was increased in cats by infusion of "mock" cerebrospinal fluid into the cisterna magna. This condition was then treated by hyperventilation. In addition to direct measurement of intracranial pressure, cerebral metabolism was assessed by near infrared spectrophotometric (niroscopic) measurement of cytochrome a,a3 redox state and the quantity of reduced and oxygenated hemoglobin in the illuminated brain. Cerebral perfusion was assessed by injection of Cardio-Green. Increased intracranial pressure resulted in the expected reduction in cytochrome a,a3,a decrease in HbO2, an increase in Hb, and a reduction of blood flow. The vasoconstriction produced by hyperventilation, while reducing intracranial pressure, produced a further reduction in cytochrome a,a3 and HbO2, with no improvement in blood flow. The data illustrate the fallacy of governing therapy solely by intracranial pressure and demonstrate the need for a direct assessment of brain metabolism. The data also demonstrate the strengths and weaknesses of niroscopy as a noninvasive monitor of the brain metabolism if applied to patients at risk for increased intracranial pressure.
Animals↗
New principles of resuscitation for brain and spinal injury.
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Brain Injuries↗
Occult esophageal perforation associated with cervical spine fracture.
A case of surgically confirmed cervical esophageal perforation associated with burst fractures of two cervical vertebral bodies is presented. We also describe a second case in which an incidentally discovered abscess of the cervical region could have been the result of esophageal perforation secondary to spine injury. Both patients had negative positive contrast esophagograms . This complication of cervical spine injury is extremely rare, and diagnosis can be difficult. Cervical esophageal perforation must be considered in the face of unexplained cervical, thoracic, or systemic sepsis and in the presence of an unexplained cervical mass. Severe cervical fracture with or without subluxation seems to constitute the anatomical basis for the entity. The treatment consists of drainage and antibiotics aimed at oral flora. The clinical features, diagnostic tests, and surgical management of this entity are reviewed.
Adult↗
Cerebral revascularization in the management of stroke.
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Cerebral Revascularization↗
Primary dural melanoma: a clinical and morphological study.
This study reviews the literature pertaining to primary meningeal melanoma and reports the clinical and ultrastructural findings in a case where the tumor appeared to be of pachymeningeal (dural) origin. This is clearly a departure from all previously described cases, in which a leptomeningeal (pial-arachnoidal) origin was either defined or assumed. Clinically, this case was remarkable in its rarity, its presentation as a cerebellopontine angle syndrome, and its occurrence in a Negro, a race in which melanomas are uncommon. Ultrastructurally, the tumor did demonstrate the presence of basement membrane abnormalities and numerous endothelial fenestrations. However, it was found to be made up of a homogenous cell population, consisting only of electron-lucent, melanin-laden cells. The mixed cell population noted previously in a primary leptomeningeal melanoma was not found in this tumor. In view of the fact that this patient continues to do well 1 1/2 years after operation, with no evidence of tumor recurrence, it is suggested that a homogenous cell population noted on electron microscopy could indicate a better prognosis. In addition, it may also indicate a pachymeningeal rather than a leptomeningeal origin for the tumor. A plea is made for greater specificity in terminology when describing primary meningeal melanomas and for a concerted effort to distinguish between those of dural and those of leptomeningeal origin.
Adult↗
Hyperkalemia associated with indomethacin.
Substantial hyperkalemia with ECG abnormalities developed in a patient. None of the common causes of hyperkalemia was found, eg, acidosis, hemolysis, rhabdomyolysis, renal failure, hypoadrenalism, leukocytosis, or thrombocytosis. The patient had been receiving indomethacin, a drug known to inhibit renin production, aldosterone excretion, and prostaglandin synthetase. The patient was rechallanged with indomethacin, and measurements of serum potassium and renin, urinary potassium, aldosterone, and creatinine levels were done. The study period clearly showed a hyporeninemic-hypoaldosterone states with diminished renal potassium excretion, leading to hyperkalemia associated with the indomethacin therapy. The development of hyperkalemia caused by indomethacin is probably unusual; however, we believe it is important to report this potentially serious pathophysiologic occurrence associated with a commonly used medication.
Adult↗
Surgical removal of bilateral papillomas of the choroid plexus of the lateral ventricles with resolution of hydrocephalus. Case report.
The authors report a patient with bilateral papillomas of the choroid plexus of the lateral ventricles with documentation of cerebrospinal fluid (CSF) hypersecretion causing hydrocephalus. Special attention is given to the large volume of CSF produced by these tumors (removal of one tumor reduced CSF outflow by one-half) and to the fact that CSF diversion was not required after both tumors were removed. Since tumor removal alone was sufficient to stop the progression of hydrocephalus, we feel that this case supports the concept that elevated CSF production by itself is sufficient to cause hydrocephalus in patients with papillomas of the choroid plexus.
Cerebral Ventricle Neoplasms↗
Significance of intracranial hypertension in severe head injury.
Measurements of intracranial pressure (ICP) were begun within hours of injury in 160 patients with severe brain trauma, and continued in the intensive care unit. Some degree of increased ICP (greater than 10 mm Hg) was present on admission in most cases (82%), and in all but two of the 62 patients with intracranial mass lesions requiring surgical decompression; ICP was over 20 mm Hg on admission in 44% of cases, and over 40 mm Hg in 10%. In patients with mass lesions only very high ICP (greater than 40 mm Hg) on admission was significantly associated with a poor neurological picture and outcome from injury, while in patients with diffuse brain injury any increase in ICP above 10 mm Hg was associated with a poorer neurological status and a worse outcome. Despite intensive measures aimed at prevention of intracranial hypertension, ICP rose over 20 mm Hg during the monitoring period in 64 of the 160 patients (40%). Postoperative increases in ICP over 20 mm Hg (mean) were seen in 52% of the patients who had had intracranial masses evacuated, and could not be controlled by therapy in half of these cases. Even in patients without mass lesions, ICP rose above 20 mm Hg in a third of the cases, despite artificial ventilation and steroid therapy. Of the 48 patients who died, severe intracranial hypertension was the primary cause of death in nearly half and even moderately increased ICP (greater than 20 mm Hg) was associated with higher morbidity in patients with mass lesions and those with diffuse brain injury. Measurement of ICP should be included in management of patients with severe head injury.
Brain Injuries↗
ICP monitoring: complications and associated factors.
1. Patients with complications when compared with those not developing a complication: a. Were older, 44.4 vs. 34.5 years; b. Were monitored longer, 14.0 vs. 6.5 days; c. Were treated with steroids longer, 18.3 vs. 10.3 days; d. Were hospitalized longer, 35.7 vs. 27.7 days; e. Are twice as likely to die; f. Average age of those dying is older, 46 vs. 30 years; g. Have no clear relationship to antibiotics; h. Do not have a preponderance of single diagnostic category to account for these differences; i. Complications were always controlled with standard therapy; j. An ICP complication was almost never responsible, per se, for death. 2. Over all complication rate was 18%; due to monitoring was 4.5 to 11.5%. 3. Monitoring was responsible for, or contributed to, 25 to 60% of the complications. 4. No complications occurred when monitoring was discontinued within 3 days. 5. Long periods of treatment with steroids increased the risk of a complication developing. 6. Long periods of monitoring were associated with an increased risk of complication. 7. "Individual" factors are partly responsible for the development of a complication, and death. 8. There are two groups of complications: "early" and "late." A. Those most likely to be monitor related occur "late" and account for 35% of the complications. B. Those developing "early" infection account for 65% of the complications and are most likely caused by factors other than monitoring. While there are complications directly attributable to monitoring, the rate is low and they are readily controlled by standard neurosurgical management. While monitoring may increase the morbidity, it does not increase the mortality. We feel that the over-all risk is small and that the returns are great--both in terms of knowledge and patient benefit.
Adult↗