Posttraumatic narcolepsy: the complete syndrome with tissue typing

1989 ◽  
Vol 71 (5) ◽  
pp. 765-767 ◽  
Author(s):  
Janine L. Good ◽  
Elizabeth Barry ◽  
Paul S. Fishman
Keyword(s):  
Brain Injury ◽  
Head Injury ◽  
Human Lymphocyte ◽  
Genetic Predisposition ◽  
Sleep Disturbances ◽  
Content Type ◽  
Lymphocyte Antigen ◽  
Tissue Typing ◽  
The Brain ◽  
Fine Print

✓ Although sleep disturbances following head injury are common, well-documented posttraumatic narcolepsy has rarely been reported. A patient with all four major features of narcolepsy following significant head injury is presented. Tissue typing revealed the presence of the human lymphocyte antigen DR2, which is strongly associated with idiopathic narcolepsy. Interaction between the brain injury and a genetic predisposition appears to be involved in the development of posttraumatic narcolepsy.

Dimethyl sulfoxide in the treatment of experimental brain compression

1973 ◽  
Vol 38 (3) ◽  
pp. 345-354 ◽  
Author(s):  
J. C. de la Torre ◽  
D. W. Rowed ◽  
H. M. Kawanaga ◽  
S. Mullan
Keyword(s):  
Brain Injury ◽  
Head Injury ◽  
Mortality Rate ◽  
Dimethyl Sulfoxide ◽  
Rhesus Monkeys ◽  
Neurological Deficits ◽  
Content Type ◽  
Brain Compression ◽  
The Brain ◽  
Fine Print

✓ Forty rhesus monkeys were subjected to acute experimental head injury by extradural balloon compression of the brain. A critical endpoint in the compression was used to inject either saline, urea, or dimethyl sulfoxide (DMSO). All saline-treated animals died. Ten of 15 urea-treated animals survived, while 14 of 15 DMSO-injected monkeys survived. The incidence of neurological deficits seen in survivors was four for urea and one for DMSO. It is concluded that DMSO is capable of modifying the mortality rate and posttraumatic sequelae of brain injury in the experimental model used.

Demonstration of massive traumatic brain swelling within 20 minutes after injury

1977 ◽  
Vol 46 (2) ◽  
pp. 256-258 ◽  
Author(s):  
Arthur I. Kobrine ◽  
Eugene Timmins ◽  
Rodwan K. Rajjoub ◽  
Hugo V. Rizzoli ◽  
David O. Davis
Keyword(s):  
Head Injury ◽  
Closed Head Injury ◽  
Brain Swelling ◽  
Axial Tomography ◽  
Content Type ◽  
Closed Head ◽  
Vascular Dilatation ◽  
Computerized Axial Tomography ◽  
The Brain ◽  
Fine Print

✓ The authors documented by computerized axial tomography a case of massive brain swelling occurring within 20 minutes of a closed head injury. It is suggested that the cause of the brain swelling is acute vascular dilatation.

Large leptomeningeal cyst of the brain

1971 ◽  
Vol 35 (5) ◽  
pp. 619-622 ◽  
Author(s):  
Adelola Adeloye
Keyword(s):  
Head Injury ◽  
Congenital Malformation ◽  
Leptomeningeal Cyst ◽  
Content Type ◽  
Post Traumatic ◽  
The Brain ◽  
Fine Print

✓ An unusually large leptomeningeal cyst of the brain is described in a 9-month-old girl who sustained a head injury at the age of 7 weeks. Although the impression was that the cyst was of the post-traumatic variety, it seemed possible that a congenital malformation of the brain antedated the head injury.

Intravascular coagulation: a common phenomenon in minor experimental head injury

1981 ◽  
Vol 54 (1) ◽  
pp. 21-25 ◽  
Author(s):  
J. Jaap van der Sande ◽  
Josephus J. Emeis ◽  
Jan Lindeman
Keyword(s):  
Head Injury ◽  
Blood Vessels ◽  
Common Phenomenon ◽  
Content Type ◽  
Intravascular Coagulation ◽  
The Brain ◽  
Fine Print

✓ Fibrin microthrombi were demonstrated by an immunoenzymehistochemical method in the small blood vessels of the lung and, to a lesser extent, in the brain in rats after minor experimental head injury. It was concluded that intravascular coagulation is a common phenomenon in head injury.

Loss of forebrain cholinergic neurons following fluid-percussion injury: implications for cognitive impairment in closed head injury

1995 ◽  
Vol 83 (3) ◽  
pp. 496-502 ◽  
Author(s):  
Richard H. Schmidt ◽  
M. Sean Grady
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Injury ◽  
Cholinergic Neurons ◽  
Nucleus Basalis ◽  
Neuron Loss ◽  
Content Type ◽  
Fluid Percussion ◽  
Concussive Injury ◽  
Fine Print

✓ Disturbances in memory, concentration, and problem solving are common after even mild to moderate traumatic brain injury. Because these functions are mediated in part by forebrain cholinergic and catecholaminergic innervation, in this study the authors sought to determine if experimental concussive injury produces detectable morphological damage to these systems. Fluid-percussion head injury, sufficient to cause a 13- to 14-minute loss of righting reflex, was produced in rats that had been anesthetized with halothane. Injury was delivered either at midline or 2 mm off midline and compared with appropriate sham-injured controls. After 11 to 15 days, the rat brains were stained in serial sections for choline acetyltransferase, tyrosine hydroxylase, dopamine β-hydroxylase, acetylcholinesterase, and nicotinamide adenine dinucleotide phosphate diaphorase. Cell counts were determined for the entire population of ventrobasal forebrain cholinergic cells. Midline injury produced a bilateral loss of cholinergic neurons averaging 36% in area Ch1 (medial septal nucleus), 45% in Ch2 (nucleus of the diagonal band of Broca), and 41% in Ch4 (nucleus basalis of Meynart), (p ≤ 0.05). Lateralized injury resulted in cholinergic neuron loss of similar magnitude ipsilaterally (p ≤ 0.05), but a smaller contralateral loss of between 11% and 28%. No loss of neurons was detected in the pontomesencephalic cholinergic groups Ch5 and Ch6. There was no visible effect of head injury on forebrain dopamine or noradrenergic innervation. A significant and apparently selective loss of ventrobasal forebrain cholinergic neurons following brief concussive injury in rats is demonstrated in this study. This type of injury is known to produce significant disturbance in cognitive tasks linked to neocortical and hippocampal cholinergic function. It remains to be determined how this neuron loss occurs, whether it can be prevented with neuroprotective agents, how it affects innervation in target tissues, and whether it occurs in human victims of traumatic brain injury.

Intracerebral microdialysis in neurointensive care: the use of urea as an endogenous reference compound

2001 ◽  
Vol 94 (3) ◽  
pp. 397-402 ◽  
Author(s):  
Elisabeth Ronne-Engström ◽  
Kristina Giuliana Cesarini ◽  
Per Enblad ◽  
Göran Hesselager ◽  
Niklas Marklund ◽  
...  
Keyword(s):  
Brain Injury ◽  
Clinical Laboratory ◽  
Subcutaneous Tissue ◽  
Intracerebral Microdialysis ◽  
Reference Compound ◽  
Content Type ◽  
Endogenous Reference ◽  
The Brain ◽  
Fine Print

Object. When evaluating the results of intracerebral microdialysis, the in vivo performance of the microdialysis probe must be considered, because this determines the fraction of the interstitial concentration obtained in the microdialysis samples. The in vivo performance is dependent on several factors, for example, the interstitial compartment's diffusion characteristics, which may vary during the course of the acute brain injury process. In the present study the authors investigated the method of controlling the in vivo performance by using urea, which is evenly distributed in all body fluid compartments, as an endogenous reference compound and by comparing the urea levels in three compartments: the brain (CNS), abdominal subcutaneous tissue (SC), and blood serum (BS). Methods. Sixty-nine patients with traumatic brain injury or cerebrovascular disease were included in the study. In 63 of these patients a CNS probe was used, an SC probe was used in 40, and both were used in 34. Urea was measured by enzymatic methods, at bedside for the microdialysis samples and in routine clinical laboratory studies for the BS samples, with the probe calibrated to give identical results. The correlation coefficient for CNS/SC urea was 0.88 (2414 samples), for CNS/BS urea it was 0.89 (180 samples), and for SC/BS urea it was 0.98 (112 samples). Conclusions. Urea levels in the CNS, SC, and BS were highly correlated, which supports the assumption that urea is evenly distributed. The CNS/SC urea ratio can therefore be used for monitoring the CNS probe's in vivo performance. Fluctuations in other substances measured with microdialysis are probably caused by biological changes in the brain, as long as the CNS/SC urea ratio remains constant.

Influence of oxygen therapy on glucose—lactate metabolism after diffuse brain injury

2004 ◽  
Vol 101 (2) ◽  
pp. 323-329 ◽  
Author(s):  
Michael Reinert ◽  
Benoit Schaller ◽  
Hans Rudolf Widmer ◽  
Rolf Seiler ◽  
Ross Bullock
Keyword(s):  
Brain Injury ◽  
Brain Tissue ◽  
Brain Metabolism ◽  
Arterial Line ◽  
Content Type ◽  
Diffuse Brain Injury ◽  
Lactate Levels ◽  
The Brain ◽  
Fine Print ◽  
Diffuse Brain

Object. Severe traumatic brain injury (TBI) imposes a huge metabolic load on brain tissue, which can be summarized initially as a state of hypermetabolism and hyperglycolysis. In experiments O2 consumption has been shown to increase early after trauma, especially in the presence of high lactate levels and forced O2 availability. In recent clinical studies the effect of increasing O2 availability on brain metabolism has been analyzed. By their nature, however, clinical trauma models suffer from a heterogeneous injury distribution. The aim of this study was to analyze, in a standardized diffuse brain injury model, the effect of increasing the fraction of inspired O2 on brain glucose and lactate levels, and to compare this effect with the metabolism of the noninjured sham-operated brain. Methods. A diffuse severe TBI model developed by Foda and Maramarou, et al., in which a 420-g weight is dropped from a height of 2 m was used in this study. Forty-one male Wistar rats each weighing approximately 300 g were included. Anesthesized rats were monitored by placing a femoral arterial line for blood pressure and blood was drawn for a blood gas analysis. Two time periods were defined: Period A was defined as preinjury and Period B as postinjury. During Period B two levels of fraction of inspired oxygen (FiO2) were studied: air (FiO2 0.21) and oxygen (FiO2 1). Four groups were studied including sham-operated animals: air-air-sham (AAS); air-O2-sham (AOS); air-air-trauma (AAT); and air-O2-trauma (AOT). In six rats the effect of increasing the FiO2 on serum glucose and lactate was analyzed. During Period B lactate values in the brain determined using microdialysis were significantly lower (p < 0.05) in the AOT group than in the AAT group and glucose values in the brain determined using microdialysis were significantly higher (p < 0.04). No differences were demonstrated in the other groups. Increasing the FiO2 had no significant effect on the serum levels of glucose and lactate. Conclusions. Increasing the FiO2 influences dialysate glucose and lactate levels in injured brain tissue. Using an FiO2 of 1 influences brain metabolism in such a way that lactate is significantly reduced and glucose significantly increased. No changes in dialysate glucose and lactate values were found in the noninjured brain.

Factors affecting excitatory amino acid release following severe human head injury

1998 ◽  
Vol 89 (4) ◽  
pp. 507-518 ◽  
Author(s):  
Ross Bullock ◽  
Alois Zauner ◽  
John J. Woodward ◽  
John Myseros ◽  
Sung C. Choi ◽  
...  
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Brain Injury ◽  
Head Injury ◽  
Neuronal Damage ◽  
Cell Swelling ◽  
Glutamate Antagonists ◽  
Content Type ◽  
Fine Print

Object. Recent animal studies demonstrate that excitatory amino acids (EAAs) play a major role in neuronal damage after brain trauma and ischemia. However, the role of EAAs in patients who have suffered severe head injury is not understood. Excess quantities of glutamate in the extracellular space may lead to uncontrolled shifts of sodium, potassium, and calcium, disrupting ionic homeostasis, which may lead to severe cell swelling and cell death. The authors evaluated the role of EEAs in human traumatic brain injury. Methods. In 80 consecutive severely head injured patients, a microdialysis probe was placed into the gray matter along with a ventriculostomy catheter or an intracranial pressure (ICP) monitor for 4 days. Levels of EAAs and structural amino acids were analyzed using high-performance liquid chromatography. Multifactorial analysis of the amino acid pattern was performed and its correlations with clinical parameters and outcome were tested. The levels of EAAs were increased up to 50 times normal in 30% of the patients and were significantly correlated to levels of structural amino acids both in each patient and across the whole group (p < 0.01). Secondary ischemic brain injury and focal contusions were most strongly associated with high EAA levels (27 ± 22 µmol/L). Sustained high ICP and poor outcome were significantly correlated to high levels of EAAs (glutamate > 20 µmol/L; p < 0.01). Conclusions. The release of EAAs is closely linked to the release of structural amino acids and may thus reflect nonspecific development of membrane micropores, rather than presynaptic neuronal vesicular exocytosis. The magnitude of EAA release in patients with focal contusions and ischemic events may be sufficient to exacerbate neuronal damage, and these patients may be the best candidates for treatment with glutamate antagonists in the future.

Impaired cerebral mitochondrial function after traumatic brain injury in humans

2000 ◽  
Vol 93 (5) ◽  
pp. 815-820 ◽  
Author(s):  
Bon H. Verweij ◽  
J. Paul Muizelaar ◽  
Federico C. Vinas ◽  
Patti L. Peterson ◽  
Ye Xiong ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Injury ◽  
Oxygen Content ◽  
Mitochondrial Function ◽  
Oxygen Delivery ◽  
Neuronal Cell ◽  
Content Type ◽  
Atp Production ◽  
Fine Print

Object. Oxygen supply to the brain is often insufficient after traumatic brain injury (TBI), and this results in decreased energy production (adenosine triphosphate [ATP]) with consequent neuronal cell death. It is obviously important to restore oxygen delivery after TBI; however, increasing oxygen delivery alone may not improve ATP production if the patient's mitochondria (the source of ATP) are impaired. Traumatic brain injury has been shown to impair mitochondrial function in animals; however, no human studies have been previously reported.Methods. Using tissue fractionation procedures, living mitochondria derived from therapeutically removed brain tissue were analyzed in 16 patients with head injury (Glasgow Coma Scale Scores 3–14) and two patients without head injury. Results revealed that in head-injured patients mitochondrial function was impaired, with subsequent decreased ATP production.Conclusions. Decreased oxygen metabolism due to mitochondrial dysfunction must be taken into account when clinically defining ischemia and interpreting oxygen measurements such as jugular venous oxygen saturation, arteriovenous difference in oxygen content, direct tissue oxygen tension, and cerebral blood oxygen content determined using near-infrared spectroscopy. Restoring mitochondrial function might be as important as maintaining oxygen delivery.

Head injury caused by underwater explosion of a firecracker

1972 ◽  
Vol 37 (1) ◽  
pp. 95-99 ◽  
Author(s):  
Arthur E. Hirsch ◽  
Ayub K. Ommaya
Keyword(s):  
Brain Injury ◽  
Head Injury ◽  
Severe Head Injury ◽  
Skull Fracture ◽  
Underwater Explosion ◽  
Content Type ◽  
Base Of The Skull ◽  
Impact Energies ◽  
Fine Print

✓ A firecracker exploded in contact with the skin and within 6 inches of the base of the skull of a young man while he was swimming underwater. The resultant severe head injury and death appeared to be directly related to the underwater explosion. Reconstruction of the mechanics of this injury indicates that when the head is subjected to impact energies between 440 to 1800 in.-lb and impact impulses between 1.8 to 3.5 lb/sec, both skull fracture and brain injury can occur.

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