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The author presents data on 168 patients: 75 during the acute period of brain concussion and 93 in the remote period of brain concussion. Age of the patients from 15 to 75 years. Drug treatment in these patients was combined with psychotherapy. Data are reported on the methods of psychotherapy including patients that suffered of concomitant chronic neurological and somatic diseases.
Examined were 317 patients with brain concussion ranging in age from 16 to 75 years. Of them in 133 (41.91%), chronic diseases (I-II degree chronic insufficiency of cerebral circulation, arterial hypertension, chronic cholecystitis, gastric and duodenal ulcer disease, chronic bronchitis, bronchial asthma) were revealed. Peculiarities of the course of brain concussion in these patients are noted. The author stresses that it is necessary to take into account chronic diseases when observing and treating the sufferers with brain concussion.
REG analysis of patients after brain concussion were analysed after obtaining them during 7 successive days after trauma. In the light of these results the author calls attention to the tendency for multiphasic changes in the tonus of cerebral arterial walls.
130 patients with brain concussion (BC) and 30 virtually healthy subjects, aged 16 to 50, were examined for the purpose of studying the influence exerted by different drugs affecting blood coagulation, fibrinolysis, lipid peroxidation (LPO) and antioxidant protection at exacerbation. Changes of hemostasis in BC were shown to be of the adaptation nature and to depend essentially on a conducted treatment. Normalized plasma components in the hemostasis system were registered in groups receiving cavinton. The drug, when used, reduced the LPO intensity and intensified the activity of dismutase superoxide on days 9-12 after trauma.
The purposes of this study were (1) to document the histopathological consequences of moderate traumatic brain injury (TBI) in anesthetized Sprague-Dawley rats, and (2) to determine whether post-traumatic brain hypothermia (30 degrees C) would protect histopathologically. Twenty-four hours prior to TBI, the fluid percussion interface was positioned over the right cerebral cortex. On the 2nd day, fasted rats were anesthetized with 70% nitrous oxide, 1% halothane, and 30% oxygen. Under controlled physiological conditions and normothermic brain temperature (37.5 degrees C), rats were injured with a fluid percussion pulse ranging from 1.7 to 2.2 atmospheres. In one group, brain temperature was maintained at normothermic levels for 3 h after injury. In a second group, brain temperature was reduced to 30 degrees C at 5 min post-trauma and maintained for 3 h. Three days after TBI, brains were perfusion-fixed for routine histopathological analysis. In the normothermic group, damage at the site of impact was seen in only one of nine rats. In contrast, all normothermic animals displayed necrotic neurons within ipsilateral cortical regions lateral and remote from the impact site. Intracerebral hemorrhagic contusions were present in all rats at the gray-white interface underlying the injured cortical areas. Selective neuronal necrosis was also present within the CA3 and CA4 hippocampal subsectors and thalamus. Post-traumatic brain hypothermia significantly reduced the overall sum of necrotic cortical neurons (519 +/- 122 vs 952 +/- 130, mean +/- SE, P = 0.03, Kruskal-Wallis test) as well as contusion volume (0.50 +/- 0.14 vs 2.14 +/- 0.71 mm3, P = 0.004).(ABSTRACT TRUNCATED AT 250 WORDS)
As many as 140 patients aged 16 to 75 years with a history of brain concussion were under observation. The observation periods were from 1 to 2 months after the acute period elapse up to 25 years. In addition to neurological examinations, the patients were subjected to echoencephalography, computer-aided tomography of the brain (38 patients), ultrasound tomoscopy of the brain (40 patients and 30 healthy subjects). It has been shown that the use of echoencephalography, computer-aided tomography and ultrasound tomoscopy of the brain makes it possible to identify, in some cases, different disorders on the part of the brain. The role of these methods in the diagnosis of brain concussion consequences increases, provided they are used combined or jointly with the data obtained during clinical examination and observation.
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The most frequent type of head injury in children is closed head trauma with brain concussion or contusion, and headache is the dominant complaint of early and late postinjury period. Because of scant number of studies on the problem of occurrence, characteristics and persistence of posttraumatic headache this study was undertaken in a group of 100 children (29 girls and 71 boys), aged 3-14 years old, 90 after brain concussion and 10 after contusion. Children with a history of injuries, central nervous system infections, with headaches before injury and chronic diseases were excluded. In 9 cases linear skull fracture was present after injury. The material was examined within one week after trauma, and then after 3, 6, and 12 months. After 3 months EEG was performed and repeated after 6 and 12 months in children with persistent headache or those without headache but with abnormal EEG results in the first examination. According to the additional diagnostic examinations, I excluded other causes of headache, besides head injury. In my observation 83% of children had headache after brain concussion and contusion. The majority--56%--had acute posttraumatic headache, but 27% of children complained of chronic headache, mainly tension type headache. Only 3% had migraine. In 21% of all group of 100 children, I noticed the headache persisting during the whole year of my observation. The important risk factor for the occurrence of posttraumatic headache were the age of child at the moment injury and the period of unconsciousness. The electroencephalographic recording still remains the important additional examination of posttraumatic consequences.