Generalized Brain Damage Research Articles

A unique brain germinal matrix involvement in cytomegalovirus infected fetuses: A retrospective neurosonographic analysis with outcome correlation.

To study the clinical significance of brain germinal matrix (GM) changes in cytomegalovirus (CMV) infected fetuses. This is a retrospective analysis. Group A; isolated GM finding, with or without lenticulostriatal vasculopathy (LSV). Group B; non-isolated lesion. Amniocentesis, urinalysis, postnatal US and developmental assessment, were obtained. Group A and B included 18 and four fetuses, respectively. In group A, mean fetal age at diagnosis was 34.3weeks (31-38weeks). In 15/18 (83.3%), the lesion was bilateral and LSV was present in 8/18 (44.4%). Small cysts appeared inside the lesion in 5/18 (27.7%). MRI was normal in 8/18 (44.4%). Subtle or inconclusive findings were reported in the remaining fetuses. Brain ultrasound was normal in 10/18 (55.5%) of newborns. In the remaining, caudothalamic cyst with or without LSV, or isolated LSV were found. All newborns are developing normally at a mean follow-up age of 33.3months (+/- 19.6 moths). In group B, all four patients requested for termination of pregnancy. Fetal CMV infection may cause focal GM changes, frequently accompanied by LSV, late in pregnancy. These changes may be isolated, or as part of a more generalized brain damage. When isolated, favorable prognosis is expected.

Traumatic brain injury-induced sleep disorders.

Sleep disturbances are frequently identified following traumatic brain injury, affecting 30%–70% of persons, and often occur after mild head injury. Insomnia, fatigue, and sleepiness are the most frequent sleep complaints after traumatic brain injury. Sleep apnea, narcolepsy, periodic limb movement disorder, and parasomnias may also occur after a head injury. In addition, depression, anxiety, and pain are common brain injury comorbidities with significant influence on sleep quality. Two types of traumatic brain injury that may negatively impact sleep are acceleration/deceleration injuries causing generalized brain damage and contact injuries causing focal brain damage. Polysomnography, multiple sleep latency testing, and/or actigraphy may be utilized to diagnose sleep disorders after a head injury. Depending on the disorder, treatment may include the use of medications, positive airway pressure, and/or behavioral modifications. Unfortunately, the treatment of sleep disorders associated with traumatic brain injury may not improve neuropsychological function or sleepiness.

The Neuropsychology of Proper Names

Abstract:The difference between common and proper names seems to derive from specific semantic characteristics of proper names. In particular, proper names refer to specific individual entities or events, and unlike common names, rarely map onto more general semantic characteristics (attributes, concepts, categories). This fact makes the link proper names have with their reference particularly fragile. Processing proper names seems, as a consequence, to require special cognitive and neural resources. Neuropsychological findings show that proper names and common names follow functionally distinct processing pathways. These pathways are neurally distinct and differently sensitive to focal or generalized brain damage, cognitive changes with age or lack of organic resources. Their precise location, depending on specific tasks, is still partly unknown.

高齢者破裂脳動脈りゅうにおける臨床像および治療方針の検討

Although the treatment of SAH has been much improved recently, the prognosis in elderly patients remains poor due to problems related to the aging. In order to consider future strategy to improve treatment results, it is important to know the character of SAH specific to elderly patients. The clinical features in 65 SAH patients aged between 70 and 88 years, treated between 1997 and 2002, were investigated. The results of clipping in the acute stage were analyzed in relation to tolerability to the active treatments in elderly patients. The effect of operation in the acute stage showed remarkable contrast in each group of clinical condition: in the severe group only 16% in their 70s and 0% in their 80s showed good recovery but in the mild group it was 84% in those in their 70s and 83% in those in their 80s, which was comparable to the outcome in younger patients. The clinical condition in patients with poor outcome was characterized by the presentation of disturbance in higher cortical function, indicating the presence of generalized damage in the brain in elderly patients. SAH in elderly patients is characterized clinically by distinction of 2 groups: one in which the effect of SAH easily resulted in generalized brain damage and the other in which patients could withstand the effect of SAH. The latter group can be treated aggressively. For the former group, treatments consisting of palliative measures such as embolization and meticulous general care are essential.

The importance of decompressive craniectomy for the management of severe head injuries.

Neurosurgical therapy aims to minimize the secondary brain damage after a severe head injury. This includes the evacuation of an intracranial space occupying bleeding, the reduction of intracranial volumes, in hematocephalus an external ventricular drainage, and the conservative therapy in order to influence an increased intracranial pressure (ICP) and a decreased p(ti)02. When conservative treatment fails to act a decompressive craniectomy might be successful in lowering ICP. From September 1997 until August 2001 we operated on 439 patients with severe head injuries. 50 patients (11%) were treated by means of a decompressive craniectomy. The prognosis after decompression depends on the clinical signs and symptoms on admission, the patients age and the existence of major extracranial injuries. Our guidelines for an indication for decompressive craniectomy after failure of conservative interventions and evacuation of space occupying hematomas include a patients age below 50 years without multiple trauma, a patients age below 30 years in the presence of major extracranial injuries, a severe brain swelling on CT scan, the exclusion of a primary brainstem lesion or injury and the intervention before irreversible brainstem damage and secondarily while monitoring ICP and p(ti)02 in an interval up to 48 hours after the accident before irreversible brainstem damage or generalized brain damage has occurred.

Deficits in decision-making in patients with aneurysms of the anterior communicating artery.

Patients with aneurysmal subarachnoid haemorrhage (SAH) secondary to ruptured anterior communicating artery aneurysms (ACoA) often suffer from neuropsychological sequelae including personality and behavioural changes. In this study, 31 patients with ruptured aneurysms of the ACoA resulting in SAH [mean age 50.9 years, NART (National Adult Reading Test) IQ 108.7] were compared with a group of 29 normal controls (mean age 51.9 years, NART IQ 109.7) on a specific task of decision-making. A similar task has been imaged previously and shown to activate regions involving the ventromedial prefrontal cortex. Patients with ACoA rupture showed no significant difference from controls on the task in their speed or quality of decision-making. They did, however, exhibit increased risk-taking behaviour, placing higher bets in a measure of the task which involved choices between actions associated with differing magnitudes of reward and punishment. ACoA patients demonstrated true risk-taking behaviour as opposed to simple impulsivity. Such a deficit in decision-making may be a result of direct damage to the orbital prefrontal cortex itself (as a result of micro-ischaemia or infarction after ACoA aneurysmal rupture) or to a disconnection in the ventromedial circuits from distant or generalized brain damage.

Consonant and Vowel Production of Right Hemisphere Patients

Recent reports of subclinical phonetic deficits in posterior and most particularly in Wernicke's aphasics have challenged the traditional dichotomy which characterized speech deficits in aphasia as anterior/phonetic and posterior/phonological. It is unclear whether the basis of the phonetic deficit in posterior aphasics reflects the fact that the speech production system extends to more posterior regions of the left hemisphere than previously thought or alternatively is the result of generalized brain damage effects. The present study explores the latter possibility by investigating the patterns of speech production in right hemisphere brain-damaged, non-aphasic patients with anterior and posterior lesions. Acoustic analyses conducted on a range of consonant and vowel parameters showed differences between the speech patterns of both anterior and posterior right hemisphere patients and that of Wernicke's aphasics. These findings suggest that the subclinical deficit of Wernicke's aphasics can not simply be ascribed to a generalized brain-damage effect and raise the possibility that the right hemisphere also plays some role, if only a minor one, in the phonetic implementation of speech.

Is There Really a Syndrome Involving the Co-Occurrence of Neurodevelopmental Disorder, Talent, Non-Right Handedness and Immune Disorder Among Children?

This paper is the first large-scale attempt to test Geschwind and Galaburda's (1985a, 1985b, 1985c) hypothesis that there should be a four-way association among neurodevelopmental disorders (NDs), special talents, non-right handedness, and immune disorders. In a sample of 11,578 children, several two-way associations were found, but not those most strongly predicted by the theory. For example, non-right handedness was not associated with NDs considered to be secondary to left hemisphere dysfunction (e.g., articulation disorder, reading disability, verbal aptitude deficits).Instead, non-right handedness was associated with NDs that involve generalized brain damage (e.g., cerebral palsy, mental retardation, and seizures). One immune disorder (asthma) was associated with one ND (attention deficit disorder); immune disorder was not associated with non-right handedness. Less than 1 % of this sample manifested the co-occurrence of any three or four of these markers. In sum, there was little evidence in support of the syndrome suggested by Geschwind and Galaburda (1985a, 1985b, 1985c).

Damage of Thalamus and Basal Ganglia in Asphyxiated Full-Term Neonates

Thalamic-striatal damage of symmetric bilateral distribution was found in four severely asphyxiated neonates born at term. Two patients showed evidence of bilateral thalamic-striatal necrosis and two showed hemorrhage of the same distribution. The four patients had a common history of prolonged asphyxia in the neonatal period combined with severe acidosis and respiratory insufficiency. The outcome was lethal in all children. Three patients survived for some time and showed additional evidence of generalized brain damage including cortical necrosis and subcortical leucomalacia and one patient was found to have intravital calcification of the putamen at 14 days of age. The appearance of thalamic-striatal damage in US, CCT and NMR imaging is discussed. Thalamic-striatal damage may not be detectable by US until several days after the initial insult. US does not permit a distinction between necrosis and hemorrhage, but CCT and NMR imaging may be successful. Only five infants with a comparable pattern of brain damage due to asphyxia have been described so far. Our own studies seem to indicate that thalamic-striatal damage is the hallmark of more widespread brain damage, and that it will be found more frequently if carefully looked for in asphyxiated neonates born at term.

Cerebral Damage Associated With Alcoholism: A Reexamination

The literature on neurophysical and neuropsychological studies of brain functioning in alcoholics is integrated and critically reviewed and analyzed with respect to three hypotheses of brain damage in alcoholics: (a) diffuse or generalized brain damage, (b) damage that is lateralized to the right hemisphere, and (c) damage to the frontal-limbic-diencephalic system. The authors conclude that while currently available evidence clearly demonstrates brain damage in alcoholics, it is not adequate unequivocally to support or refute any specific hypothesis of brain damage due to alcoholism. They emphasize the need for further research for both theoretical and practical purposes.

The modified word learning test and the aged psychiatric patient.

This paper reports primarily the use of the MWLT (Walton and Black, 1957) on aged subjects with a variety of clinical conditions. Earlier studies by Walton (1958), Walton, White, Black and Young (1959) and Walton and Mather (1961) demonstrated that the MWLT identified over 80 per cent. of organics without any misclassification of non-organics. More recently, Orme, Lee and Smith (1964) found that 81 per cent. of organics were correctly classified, but only 69 per cent. of non-organics. Misclassification was particularly serious with schizophrenics (70 per cent.). Other reports, including Newcombe and Steinberg (1964), White and Knox (1965), have found as few as 47 per cent. of the organic group correctly classified. These recent studies cast some doubt upon the original claims of the MWLT as a diagnostic test of generalized brain damage. We hope to present further evidence on the efficiency of the MWLT; particularly on its use with elderly subjects.

Brain damage and emotional behaviour: The effects of scrapie on the emotional responses of mice

The emotional behaviour of three groups of mice suffering from differential development of scrapie, a generalized brain damage disorder, and a normal group were investigated using the open-field test technique. Results showed that the more advanced the neuropathological process the less emotionally responsive the animals became. The correlation between emotional behaviour and the development of generalized brain damage was a highly significant negative one and the differences in emotional behaviour and neuropathological development were significant between the groups. Ambulatory activity was not significantly different between the groups, but suggested a U-shaped relationship between emotionality and brain damage.

An experimental analysis of the behavioral disturbance produced by a left frontal arachnoidal endothelioma (meningioma)

A patient with a left frontal arachnoidal endothelioma was examined at the bedside. A series of simple tasks was administered. These showed: 1. (1) An inability to carry out compounded instructions whether these were given verbally or presented as a visual model. 2. (2) An inability to carry out “symbolic” instructions. 3. (3) These incapacities did not depend on any difficulty in apprehending the instructions per se. 4. (4) Error utilization appeared related to ease of disequilibration as tested by the orienting reaction. These results are believed to be indicative of frontal lobe impairment despite the presence of more generalized brain damage which may serve to bring out in relief and carricature the essence of a disturbance produced by the local lesion.

IDIOPATHIC HYPONATREMIA IN AN INFANT WITH DIFFUSE CEREBRAL DAMAGE

A female infant, 5 months of age, with evidence of diffuse cerebral damage was found to have hyponatremia in the course of ordinary investigation. Measurements of total body chloride by the thiocyanate-space method at widely different concentrations of chloride in the serum yielded results within the expected normal range. The infant was unable to excrete an acute water load as rapidly as normal infants. Serum from the patient during a hyponatremic phase showed significantly greater antidiuretic activity than that of a normal child. We concluded that the hyponatremia was due to dilution of body fluids secondary to water retention on the basis of disturbed renal function. The hyponatremia was resistant to correction by administration of salt or mineralo-corticoids. A relation between fluid intake and concentration of sodium in the serum was demonstrated which suggested that on normal fluid intakes the child was unable to excrete solute-free water in a normal manner. This may represent the result of damage to the cerebral osmoreceptors as part of generalized brain damage. The data do not support the concept that the hyponatremia resulted from true salt-wasting, either cerebral or renal in mediation. If correction of such a state is desirable, the most useful therapeutic measure would appear to be limitation of the intake of fluid to slightly more than the amount needed to cover water expenditure from insensible losses, obligatory urine volume and growth requirements.