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At least 199 records · Page 11Linked to original sources
PubMed1987

[Complete neurological recovery after major neonatal acidosis].

After a severe fetal asphyxia, an hypotrophic (PN: 2,500 g) full-term newborn had a very poor Apgar score (1 after 1 min) and intensive resuscitation was necessary. The first arterial blood gas analysis at 1 h of life showed a profound metabolic acidosis (pH: 6.7; base defect: -30) and refractory hypoxemia (PaO2: 11 mmHg; FiO2 = 1). In a first time, the outcome was favourable after the correction of acidosis and treatment with tolazoline of a persistent fetal circulation. The depressed cerebral function symptoms disappeared within a few days; a grade I subependymal haemorrhage disappeared also rapidly. At 22 months of age, the infant had no significant developmental abnormality.

Acidosis↗
PubMedDate not supplied

Persistence of sympathetic spectral component of heart rate variability was associated with neurological recovery in severe head injury. Case report.

OBJECTIVE: To report a case of a patient affected by severe head injury where sympathetic and parasympathetic activity was evaluated by measurements of spectral analysis of heart rate variability, in serial determinations. The sympathetic component of the power spectrum never disappeared, despite signs of brain stem damage. SETTING: Intensive Therapy Unit of a University Hospital (J. Radcliffe Hospital, Oxford, England). INTERVENTIONS: None. MEASUREMENTS: Electrocardiogram, 256 R-R intervals for each step and respiration obtained by impedance plethysmography. The signals were recorded on FM tape and then digitized off-line by an analogic-to-digital converter. A program processed the signals identifying the peak of each R wave and obtaining the R-R interval (tachogram) and the Power Spectrum by Fourier transformation and autoregressive analysis. CONCLUSIONS: Persistence of sympathetic activity of Heart Rate Variability Power Spectrum indirectly reflected the integrity of the vasomotor centres allocated in the brain stem and was associated with good outcome.

Adult↗
PubMed1998

[Hyperbaric oxygenation and neurological recovery in children with organic brain damage].

INTRODUCTION AND OBJECTIVE: In order to determine the effects of hyperbaric oxygenation, 14 Cuban children (8 boys and 6 girls) with affected lesions on the Central Nervous System (CNS), were prospectively studied between September 1994 and September 1995; the patients came from the external consultation of Neuropediatric of the Academic Pediatrics Hospital, Tuna Martyrs, Cuba. PATIENTS AND METHODS: They were evaluated from the neuropediatric and neurophysiologic point of view and submitted to treatment with hyperbaric oxygenation (HBO). Five patients showed a injury to the CNS by severe asphyxia, seven by generalized infections of CNS, one patient with cerebral damage by craneoencephalic traumatism and other with vasoclusive cerebral crisis of siclemic. The average age of the children was of 4.8 +/- 3.4 years. The symptoms and signs were depending on the type on cerebral damage and its evolution. 100% of the children presented infantile cerebral paralysis (ICP) and epilepsy, most of the children were in treatment with antiepileptic drugs, buy they weren't balanced. RESULTS AND CONCLUSIONS: Satisfactory response was observed in patients that were oxygenated within the first year of the lesion, with better and faster results.

Brain Diseases↗
PubMed1985

Isolated deafness following recovery from neurologic injury and adult respiratory distress syndrome. A sequela of intercurrent aminoglycoside and diuretic use.

We report two children who survived neurologic injury (near-drowning and Reye's syndrome) and adult respiratory distress syndrome and who required prolonged ventilatory support. Follow-up examination in both children showed steady neurologic recovery, but five months following discharge from their acute illness, profound hearing loss was diagnosed in both children. A review of the literature is reported and the hypothesis that combined aminoglycoside antibiotic and loop diuretic therapy caused the hearing loss is presented. Recommendation is made for audiologic assessment within six months of recovery from critical illness of pediatric patients in whom therapy has included loop diuretic and aminoglycoside antibiotic therapy.

Aminoglycosides↗
PubMedDate not supplied

Correction of spinal instability and recovery of neurologic loss following cervical vertebral body replacement. A case report.

While replacement of cervical vertebral bodies may be required when they are compromised by infection, tumor, or injury, or when they impinge on the neural elements, this procedure does not add immediate stability and may cause additional problems. In this case, displacement of a large fibular graft into the spinal canal appeared to cause additional spinal cord and nerve root injury. Despite a long delay, decompression and firmly fitted and wired anterior and posterior grafts seemed to enhance the neurologic recovery and permitted rapid mobilization. The diagnostic value of computerized tomography is also demonstrated.

Adolescent↗
PubMed2002

LF 16-0687 Ms, a bradykinin B2 receptor antagonist, reduces brain edema and improves long-term neurological function recovery after closed head trauma in rats.

Bradykinin is an endogenous inflammatory agent that enhances vascular permeability and produces tissue edema. We investigated whether LF 16-0687 Ms, a potent nonpeptide antagonist of bradykinin type-2 (B(2)) receptor, was able to reduce brain swelling and to improve the recovery of neurological function following closed head trauma (CHT) in rats. In dose-effect studies, LF 16-0687 Ms doses of 0.75-4.5 mg/kg given 1 h after trauma significantly reduced the development of edema in the injured hemisphere by a maximum of 70%. It had no effect on the brain water content of sham-operated rats. LF 16-0687 Ms also significantly improved neurological recovery evaluated by a Neurological Severity Score (NSS) based on motor, reflex, and behavioral tests. In time-window studies LF 16-0687 Ms (2.25 mg/kg) was given 1, 2, 4, and 10 h after CHT. The extent of edema was significantly reduced when LF 16-0687 Ms was given 1 h (-45%), 2 h (-52%), and 4 h (-63%) but not 10 h (-24%) after CHT. Given at any time-point, LF 16-0687 Ms significantly improved the recovery of the NSS at 24 h. In duration of treatment studies, rats tended to recover normal neurological function over 14 days after CHT. However, time to recovery was longer in severely than in moderately injured animals, unless they were treated with LF 16-0687 Ms. This study provides further evidence that blockade of bradykinin B(2) receptors represents a potential effective approach to the treatment of focal cerebral contusions.

Animals↗
PubMed2000

Chronic relapsing thrombocytopenic purpura with severe neurological manifestations and full recovery.

Neurological complications in thrombotic thrombocytopenic purpura (TTP) are associated with poor prognosis and/or permanent damage. We report a young woman in whom the diagnosis of TTP was difficult because cardinal manifestations were absent at presentation. The patient relapsed, showing severe and dramatic neurological manifestations, including coma. She was treated with multiple therapeutic modalities and recovered fully with no neurological sequelae. The difficulties involved in the management of chronic relapsing TTP are discussed. In the absence of clear guidelines, patients are still subjected to different treatment modalities according to the personal opinions and approaches of physicians. Clearly, well-controlled clinical trials to address this problem are required.

Adult↗
PubMed2004

Differentiating midazolam over-sedation from neurological damage in the intensive care unit.

INTRODUCTION: Midazolam is used routinely to sedate patients in the intensive care unit (ICU). We suspected that midazolam over-sedation was occurring in the ICU of the Guy's and St. Thomas' Trust and that it could be difficult to differentiate this from underlying neurological damage. A sensitive assay for detecting midazolam and 1-hydroxymidazolam glucuronide (1-OHMG) in serum was developed and applied in the clinical setting. METHODS: In the present study we evaluated a series of cases managed in a mixed medical, surgical and trauma ICU. Serum was collected from 26 patients who received midazolam, were 'slow to wake' and in whom there was suspicion of neurological damage. Patient outcome was followed in terms of mortality, neurological recovery and neurological damage on discharge. RESULTS: Out of 26 patients, 13 had detectable serum levels of midazolam and/or 1-OHMG after a median of 67 hours (range 36-146 hours) from midazolam cessation. Of these 13 patients in whom midazolam/1-OHMG was detectable, 10 made a full neurological recovery. Of the remaining 13 patients with no detectable midazolam/1-OHMG, three made a full neurological recovery; 10 patients were subsequently found to have suffered neurological damage (P < 0.002), eight of whom died and two were discharged from the ICU with profound neurological damage. CONCLUSION: These findings confirm that prolonged sedation after midazolam therapy should be considered in the differential diagnosis of neurological damage in the ICU. This can be reliably detected by the assay method described. The effects of midazolam/1-OHMG persist days after administration of midazolam has ceased. After prolonged sedation has been excluded in this patient group, it is highly likely that neurological damage has occurred.

APACHE↗
PubMed1992

[The neurological outcome in patients with acute cervical spinal cord injury].

UNLABELLED: Twenty-three patients (twenty males and three females) with acute cervical spinal cord injury were cared for within a defined protocol and followed for 14 to 589 days (mean. 133 days). We evaluated the relationship between neurological recovery and neurological examination, myelography (MLG), CT-myelography (CTM) on admission. All of them were admitted to Kitasato University Hospital within 24 hours after injury. Thirteen of the 23 patients had complete injury, and the others had incomplete injury. RESULT: Four factors were found to be related to neurological recovery. They included: 1) complete injury; 2) areflexia; 3) cord swelling on CTM; and 4) complete block on MLG. Fourteen of 15 patients who had at most two of the four factors improved. But, no patients with three or four factors improved. CONCLUSION: These four factors have been recognized as indicators of bad neurological outcome. However, our result indicates that by our result, improvement of neurological function can be expected in patients affected by only one or two of these four factors. In other words these four factors have prognostic value for predicting the neurological outcome after acute cervical spinal cord injury.

Acute Disease↗
PubMed1998

New concepts for drug therapy after stroke. Can we enhance recovery?

Neurologic functions improve in most patients days and weeks after onset of a stroke. This can not be explained by recovery of the early salvageable ischemia zone. The most likely mechanism is relearning, a process in which healthy brain takes over functions lost with the infarct. Experimental studies indicate that this recovery can be modulated by pharmacological agents. NMDA antagonists and GABA agonists found to reduce infarct size in stroke models may have a harmful effect on relearning and neurologic recovery. This should be considered when clinical trial protocols are designed.

Cerebrovascular Disorders↗
PubMed2005

Delayed therapy of experimental global cerebral ischemia with acetyl-L-carnitine in dogs.

Acetyl-L-carnitine (ALCAR), when administered immediately following restoration of spontaneous circulation (ROSC) from experimental cardiac arrest (CA) has previously been demonstrated to promote normalization of brain energy metabolism and neurologic recovery following 10 min CA. In order to determine ultimate efficacy for this or other drugs, clinical trials must be performed in human subjects. In several human clinical trials, though, drug administration has been significantly delayed following resuscitation from CA. These experiments test the hypothesis that post-resuscitative delay in ALCAR administration will impair the ability of this drug to promote neurologic recovery. Neurological deficit scoring (23 h) as well as frontal cortex lactate levels (2 and 24 h) were compared following resuscitation from 10 min CA in dogs receiving either ALCAR or drug vehicle 30 min following ROSC. Dogs treated with ALCAR 30 min following ROSC from 10 min CA exhibited more normal cerebral cortex lactate levels than did vehicle control animals. There was no difference, however, in neurologic deficit scores between groups, with all animals demonstrating moderate to severe clinical neurologic impairment at 23 h following ROSC. A 30-min delay in ALCAR administration following ROSC from 10 min CA impairs the ability of this drug to promote neurologic recovery despite apparent normalization of brain lactate levels.

Acetylcarnitine↗
PubMed2005

Hypothermia for neuroprotection after cardiac arrest: systematic review and individual patient data meta-analysis.

OBJECTIVE: Only a few patients survive cardiac arrest with favorable neurologic recovery. Our objective was to assess whether induced hypothermia improves neurologic recovery in survivors of primary cardiac arrest. DATA SOURCE: Studies were identified by a computerized search of MEDLINE, EMBASE, CINAHL, PASCAL, the Cochrane Controlled Trial Register, and BIOSIS. STUDY SELECTION: We included randomized and quasi-randomized, controlled trials of adults who were successfully resuscitated, where therapeutic hypothermia was applied within 6 hrs after arrival at the emergency department and where the neurologic outcome was compared. We excluded studies without a control group and studies with historical controls. DATA EXTRACTION: All authors of the identified trials supplied individual patient data with a predefined set of variables. DATA SYNTHESIS: We identified three randomized trials. The analyses were conducted according to the intention-to-treat principle. Summary odds ratios were calculated using a random effects model and translated into risk ratios. More patients in the hypothermia group were discharged with favorable neurologic recovery (risk ratio, 1.68; 95% confidence interval, 1.29-2.07). The 95% confidence interval of the number-needed-to-treat to allow one additional patient to leave the hospital with favorable neurologic recovery was 4-13. One study followed patients to 6 months or death. Being alive at 6 months with favorable functional neurologic recovery was more likely in the hypothermia group (risk ratio, 1.44; 95% confidence interval, 1.11-1.76). CONCLUSIONS: Mild therapeutic hypothermia improves short-term neurologic recovery and survival in patients resuscitated from cardiac arrest of presumed cardiac origin. Its long-term effectiveness and feasibility at an organizational level need further research.

Heart Arrest↗
PubMed1995

Spinal cord compression by primary non-Hodgkin's lymphoma.

Epidural Cord Compression (ECC) by primary lymphomas is rare entity and constitutes less than 3% of total malignant lymphoma with Non-Hodgkin's Lymphoma (NHL), diffuse large cell type being the most common histological subtype. In this paper 16 cases of primary NHL with cord compression seen at the Department of Medical Oncology, during the period 1988-1990 are reviewed. At presentation all patients had undergone Laminectomy with decompression of epidural mass. The histological diagnosis of NHL was subclassified according to the International working formulation and was evaluated for disease process elsewhere in the body. All patients with ECC by lymphoma received high dose steroids with concurrent Radiotherapy (local) and combination Chemotherapy. These patients had longer duration of neurological deficit prior to treatment had poor response. After 6 courses of chemotherapy 50% of the patients had complete neurological recovery (CR), 31% had partial neurological recovery (PR) and in 19% there was no neurological recovery (NR).

Adolescent↗
PubMed1981

Cerebrospinal fluid and serum creatine kinase BB activity after out-of-hospital cardiac arrest.

In patients resuscitated from out-of-hospital cardiac arrest, neurologic outcome was compared with creatine kinase isoenzyme BB activity (CKBB) in cerebrospinal fluid (CSF) in 20 patients and in serum in 52 patients. CSF CKBB was 2 units per liter or less in patients with complete neurologic recovery but was significantly elevated in patients without neurologic recovery (mean, 55 units per liter) or with incomplete neurologic recovery (mean, 7 units per liter). Serum CKBB was detected more than 6 hours after cardiac arrest in only 4% of patients with complete neurologic but in all patients without neurologic recovery. These results demonstrate a relationship between CSF and serum CKBB and neurologic outcome after cardiac arrest.

Brain Injuries↗