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PubMed1984

High blood glucose level on hospital admission and poor neurological recovery after cardiac arrest.

To evaluate the relationship between blood glucose and neurological recovery after cardiac arrest, we retrospectively reviewed our experience with 430 consecutive patients resuscitated after out-of-hospital cardiac arrest. All these patients had received variable amounts of intravenous 5% glucose solutions before admission. Awakening patients, those following commands or having comprehensible speech, were classified as to whether they suffered persistent neurological deficits. The mean blood glucose level on hospital admission was higher in 154 patients who never awakened than in 276 who did awaken (mean, 341 versus 262 mg per 100 milliliters; p less than 0.0005). Among the 276 who awakened, 90 patients with persistent neurological deficits had higher mean glucose levels on admission than did 186 without deficits (286 versus 251 mg per 100 milliliters; p less than 0.02). These significant differences persisted after excluding all patients whose glucose levels were higher than 500 mg per 100 milliliters and after controlling for potentially confounding variables using multiple regression analysis.

Blood Glucose↗
PubMed2004

Neurological recovery and its influencing factors in thoracic and lumbar spine fractures after surgical decompression and stabilization.

Surgical decompression and internal fixation of the injured spine have become standard procedures in the management of thoracic and lumbar spine fractures, but their effectiveness on neurological recovery remains controversial. We report on 169 consecutive patients with thoracic and lumbar spine fractures who were treated by reduction, fusion, and internal fixation using transpedicular screw-rod systems. Open decompression was carried out in 67 (39.6%) of them, including all 42 patients (25%) who presented with initial neurological deficits. At least 8 months following surgery, 30 (71%) had neurologically improved by one to three grades on the Frankel scale. Thirteen (59%) out of 22 patients whose initial deficits had been classified as "motor useless" (Frankel grades A to C) could walk, at least with support. Thirteen out of 20 patients with posttraumatic deficit Frankel D ("motor useful") improved to full recovery (Frankel E). In six (3.6%) patients (all from the group of the 127 patients without initial neurological deficits), permanent slight postoperative neurological impairment of one Frankel grade (E to D) was seen, among them two (1.2%) with new minor motor deficit. Neurological outcome was significantly better (p<0.01) in patients operated upon within the first 24 h after injury than in those who underwent surgery later. Severity of injury also had a negative influence (p<0.001) on neurological recovery. Analysis suggests that there may be significant neurological improvement in patients treated surgically very early.

Adolescent↗
PubMed2006

Quantitative EEG and neurological recovery with therapeutic hypothermia after asphyxial cardiac arrest in rats.

We test the hypothesis that quantitative electroencephalogram (qEEG) can be used to objectively assess functional electrophysiological recovery of brain after hypothermia in an asphyxial cardiac arrest rodent model. Twenty-eight rats were randomly subjected to 7-min (n = 14) and 9-min (n = 14) asphyxia times. One half of each group (n = 7) was randomly subjected to hypothermia (T = 33 degrees C for 12 h) and the other half (n = 7) to normothermia (T = 37 degrees C). Continuous physiologic monitoring of blood pressure, EEG, and core body temperature monitoring and intermittent arterial blood gas (ABG) analysis was undertaken. Neurological recovery after resuscitation was monitored using serial Neurological Deficit Score (NDS) calculation and qEEG analysis. Information Quantity (IQ), a previously validated measure of relative EEG entropy, was employed to monitor electrical recovery. The experiment demonstrated greater recovery of IQ in rats treated with hypothermia compared to normothermic controls in both injury groups (P < 0.05). The 72-h NDS of the hypothermia group was also significantly improved compared to the normothermia group (P < 0.05). IQ values measured at 4 h had a strong correlation with the primary neurological outcome measure, 72-h NDS score (Pearson correlation 0.746, 2-tailed significance <0.001). IQ is sensitive to the acceleration of neurological recovery as measured NDS after asphyxial cardiac arrest known to occur with induced hypothermia. These results demonstrate the potential utility of qEEG-IQ to track the response to neuroprotective hypothermia during the early phase of recovery from cardiac arrest.

Animals↗
PubMed1998

The natural course of neurological recovery following cardiopulmonary resuscitation.

In 231 patients resuscitated from circulatory arrest of cardiovascular or pulmonary aetiology brain recovery was evaluated by serial neurological and EEG examinations for up to 1 year. One-hundred and sixteen patients never regained consciousness; 115 patients awakened within 30 days, and 40 eventually recovered completely within 90 days. Patients who had electrocortical activity recorded by the immediate post-resuscitation EEG (N = 106), and patients initially without such activity (N=125) pursued the same course of recovery: during unconsciousness, interrelated EEG and neurological findings featured a phase of intermittent cortical activity with postural or stereotypic motor responses followed by a phase of continuous cortical activity with sequential appearances of delta, theta, and alpha activities on EEG accompanied by stereotypic or defensive motor responses. After awakening, the sequential return of motor, sensory, and mental faculties differentiated an early phase of severe disability with orientating eye movements and a bilateral Babinski response from the phase of moderate disability featured by speech, locomotor functions, ability to cope with personal necessities and orientation as to personal data, and a normal plantar response. Finally, orientation as to time, place and role of other persons, and retention and recall, defined the phase of slight/no disability. Abnormal courses were identified by incomplete EEG and neurological recoveries or by the appearance of spikes and sharpwaves in the EEG, or by losses of function.

Brain↗
PubMed1997

An evaluation of the factors affecting neurological recovery following spinal cord injury.

We reviewed 71 consecutive spinal cord injuries to determine the factors influencing neurological recovery. Sixty-three (35 tetraplegics and 28 paraplegics) were available for follow-up at a mean of 29.6 months. The American Spinal Injury Association (ASIA) scoring system was used on admission and at follow-up to determine change in neurological status. Treatment with corticosteroids or surgical intervention had no significant effect on outcome. Tetraplegics, both complete and incomplete, had a significantly better outcome than paraplegics (p < 0.02). Incomplete cord injury carried a better prognosis of motor recovery (p < 0.0001). Pattern of injury was an important determinant of recovery in the complete tetraplegia group. We conclude that many factors influence recovery following spinal cord injury and the effect of treatment may be difficult to demonstrate.

Adolescent↗
PubMed1991

1991 Volvo Award in experimental studies. Cauda equina syndrome: neurologic recovery following immediate, early, or late decompression.

An animal model of cauda equina syndrome was developed. Neurologic recovery was analyzed following immediate, early, and delayed decompression. Five experimental groups, each containing six dogs, were studied. Compression of the cauda equina was performed in all 30 dogs following an L6-7 laminectomy. The cauda equina was constricted by 75% in each group. The first group was constricted and immediately decompressed. The remaining groups were constricted for 1 hour, 6 hours, 24 hours, and 1 week, respectively, before being decompressed. Somatosensory evoked potentials were performed before and after surgery, before and immediately after decompression, and 6 weeks following decompression. Daily neurologic exams using the Tarlov grading scale were performed. At 6 weeks postdecompression, all dogs were killed, and the neural elements analyzed histologically. Following compression, all 30 dogs had significant lower extremity weakness, tail paralysis, and urinary incontinence. All dogs recovered significant motor function 6 weeks following decompression. The dogs with immediate decompression generally recovered neurologic function within 2-5 days. The dogs receiving 1-hour and 6-hour compression recovered within 5-7 days. The dogs receiving 24-hour compression remained paraparetic 5-7 days, with bladder dysfunction for 7-10 days and tail dysfunction persisting for 4 weeks. The dogs with compression for 1 week were paraparetic (Tarlov Grade 2 or 3) and incontinent during the duration of cauda equina compression. They recovered to walking by 1 week and Tarlov Grade 5 with bladder and tail control at the time of euthanasia. Immediately after compression, all five groups demonstrated at least 50% deterioration of the posterior tibial nerve evoked potential amplitudes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

Psychosocial outcomes at 18 months after good neurological recovery from aneurysmal subarachnoid haemorrhage.

OBJECTIVES: To evaluate functioning, 18 months after surgery, of 49 patients with good neurological recovery following aneurysmal subarachnoid haemorrhage (SAH), and to determine the extent of any improvements in disturbances of mood, cognitive functioning, and levels of activity and participation previously observed at 9 month follow up. METHODS: SAH patients, matched for age, gender, and occupation with healthy control participants, completely quantitative measures of mood (HADS, FIES, BDI) and activity/participation (BICRO-39 scales), and a brief cognitive assessment battery (verbal fluency, digit span, prose recall). Controls completed the HADS and the BICRO-39. RESULTS: Patients showed some recovery of cognitive functioning, though impairments of prose recall persisted. Anxiety and depression symptoms were higher in patients than in controls, but fewer than 20% scored in the clinical range on any questionnaires except for RIES-Intrusive thoughts (22%); only three showed signs of full blown post-traumatic stress disorder. Almost half showed elevated dependence on others for domestic activities and organisation and abnormally low levels of employment. Very little variance in outcome was predicted by demographic variables, neurological or cognitive impairment, prior life stress, or mood. However, levels of social activity and self-organisation were related to persisting fatigue. CONCLUSIONS: The observed decline in intrusive thoughts and avoidance over time is consistent with that seen after life threatening illness or trauma. The persistent reductions in independence and levels of employment may in some cases reflect considered lifestyle adjustments rather than adverse and unwanted changes but in others indicate a need for focused rehabilitation.

Activities of Daily Living↗
PubMed1983

Traumatic decerebrate rigidity and neurological recovery: a case report.

Trauma is the most common cause of decerebrate rigidity (DR). DR has been incorrectly equated with extensor posturing alone, however, and the "classical" criteria of decerebration generally have not been incorporated in the neurological evaluation of head-injured patients. A high mortality rate is associated with extensor posturing in head injury, and there have been few reports detailing neurological recovery and the quality of survival of patients with traumatic DR. The criteria of Sherrington are applied to a case of DR caused by midbrain injury, accompanied by mild, diffuse, hemispheric white matter changes shown on computed tomographic scan. The neurological examination and recovery are discussed. The literature is reviewed and the potential of DR in the prognosis of head injury is suggested.

Adult↗
PubMed1986

Nicardipine increases cerebral blood flow but does not improve neurologic recovery in a canine model of complete cerebral ischemia.

The effects of the calcium entry blocker nicardipine on CBF, CMRO2, and neurologic outcome following 10 min of complete cerebral ischemia were examined in dogs. In CBF and CMRO2 studies, the CBF in the untreated group (seven dogs) and the nicardipine group (seven dogs; 20 micrograms kg-1 at 30 min postischemia and a subsequent infusion of 2 micrograms kg-1 min-1 for 90 min) initially increased to 300-400% and then returned to preischemic values at 30 min postischemia. Thereafter the CBF in the untreated group significantly decreased to 50% of preischemic values for the following 90-min period (hypoperfusion), while the CBF in the nicardipine group did not differ from preischemic values. The CMRO2 in both groups decreased to approximately 50-80% of preischemic values after 15 min postischemia and did not differ between the groups throughout the study. In neurologic outcome studies, 18 dogs were divided into three groups (of six dogs each): untreated; saline infusion only, posttreated; nicardipine as in CBF and CMRO2 studies, pretreated; nicardipine 20 micrograms kg-1 at 2 min preischemia and a subsequent infusion of 2 micrograms kg-1 min-1 from immediately postischemia to 120 min postischemia. Nicardipine treatment initiated either before or after ischemia failed to improve neurologic outcome at 48 h postischemia. Thus, the increase of postischemic global CBF by nicardipine is not accompanied by neurologic recovery in a canine model of complete cerebral ischemia.

Animals↗
PubMed1992

Efficacy of the 21-aminosteroid U74006F in improving neurological recovery after spinal cord injury in rats.

The efficacy of three different regimens of the 21-aminosteroid U74006F in counteracting the neurological damage after spinal cord compression causing paraparesis in rats was investigated. Three groups of ten animals each were given totally 6 mg/kg of U74006F in different regimens beginning one hour after injury (A: bolus doses of 1.5 mg/kg at 1, 4, 7 and 10 hours; B: bolus of 1.5 mg/kg at 1 hour and 4.5 mg/kg as an infusion over the next 9 hours; and C: infusion alone, 6 mg/kg, given between 1 and 10 hours after trauma). Two groups of ten animals each received vehicle alone in administration modes comparable to those of the U74006F treated animals. The motor function was assessed daily on the inclined plane. On day one, the capacity angle had decreased from about 62 degrees preoperatively to 28-30 degrees in the two vehicle-treated groups and in group C. In these groups there was a similar improvement in neurological function and on day 9 the capacity angles were 49-55 degrees. In groups A and B, both of which received a bolus dose of U74006F at 1 hour, the neurological outcome improved on day one with capacity angles of 38-40 degrees. The difference in neurological function between the animals given U74006F as bolus doses and those given vehicle alone persisted over the entire observation span until day 9. The data suggest that early treatment with a bolus dose seems to be required in order to obtain an effect of U74006F on neurological recovery.

Animals↗
PubMed2000

Endothelin type A-antagonist improves long-term neurological recovery after cardiac arrest in rats.

OBJECTIVE: Antagonists of endothelin (ET(A)) receptors improve postischemic hypoperfusion. In this study we investigated whether the selective ET(A)-antagonist BQ123 also improves postischemic functional recovery. STUDY DESIGN: Cardiac arrest of 12 mins duration was induced in rats by electrical fibrillation of the heart, followed by advanced cardiopulmonary resuscitation. BQ123 (0.8 mg/kg; n = 9) or its vehicle (saline; n = 9) was injected intravenously at 15 mins after the return of spontaneous circulation. The neurologic deficit was scored daily for 7 days after resuscitation by rating consciousness, various sensory and motor functions, and coordination tests. On day 7, we measured functional coupling of cerebral blood flow under halothane anesthesia by recording laser-Doppler flow during electrical forepaw stimulation, and we measured vascular reactivity to CO2 by measuring the laser-Doppler flow change during ventilation with 6% CO2. The brains were perfusion-fixated with 4% paraformaldehyde, and the histopathologic damage was evaluated in the CA1 sector of hippocampus, in the motor cortex, and in the cerebellum. RESULTS: Treatment with BQ123 had no effect on histopathologic damage, but it significantly improved neurologic recovery. In all nine treated rats, neurologic performance returned to near normal within 2 days whereas four of nine untreated animals developed spastic paralysis of the hind limbs and severe coordination deficits. BQ123 also normalized CO2 reactivity and improved the functional cerebral blood flow response to somatosensory stimulation. CONCLUSIONS: The ET(A)-antagonist BQ123 significantly improves neurologic outcome after 12 mins of cardiac arrest. The apparent restoration of vascular reactivity demonstrates a correlation between hemodynamic factors and functional recovery.

Animals↗
PubMed1985

High-dose glucocorticoid treatment improves neurological recovery in head-injured mice.

The ability of a single large intravenous dose of the sodium succinate esters of the glucocorticoids methylprednisolone, prednisolone, or hydrocortisone to enhance early neurological recovery after moderate to severe blunt head injury was examined in male CF-1 mice. Unanesthetized mice were restrained and subjected to a 900 gm-cm head injury produced by a 50-gm weight dropped 18 cm. This injury resulted in immediate loss of consciousness (loss of the righting reflex) in all animals, and death in approximately 30%. Survivors received a 0.1-ml tail vein injection of either vehicle or 15, 30, 60, or 120 mg/kg of methylprednisolone, prednisolone, or hydrocortisone within 5 minutes. Their neurological status was evaluated at 1 hour after injury. A 30-mg/kg dose of methylprednisolone was found to improve recovery significantly in comparison to that seen in vehicle-treated mice. A 15-mg/kg dose was less effective, and a 60- or 120-mg/kg dose was essentially ineffective. Prednisolone was also observed to improve neurological scores at 1 hour postinjury. A 60-mg/kg dose of prednisolone was optimal, while lower and higher doses had no effect. Hydrocortisone was unable to improve recovery over the wide dose range tested. The implications of these findings for the clinical management of head injury with glucocorticoid steroids are discussed.

Animals↗
PubMed1985

Beneficial effects of acute intravenous ibuprofen on neurologic recovery of head-injured mice: comparison of cyclooxygenase inhibition with inhibition of thromboxane A2 synthetase or 5-lipoxygenase.

The ability of the cyclooxygenase inhibitor ibuprofen to affect early neurologic recovery following a moderately severe concussive head injury was studied in male CF-1 mice. Each mouse received a 900 g-cm (50 g weight dropped 18 cm) head injury, followed within 5 minutes with a single IV dose of ibuprofen (sodium salt; 1, 3, 10, or 30 mg/kg). At 1 hour postinjury, their neurologic status was assessed using a grip test. Drug administration and neurologic evaluation were carried out blindly. A dose-related improvement in recovery was observed, with a 10 mg/kg IV dose causing a 122% increase in the mean grip test score compared to 0.9% saline treatment (p less than 0.01 by one-way ANOVA). In addition, there was a significant decrease in the number of mice in the 10 mg/kg ibuprofen group that fell off the grip test string in 0-5 seconds (i.e., that were severely impaired). In comparison, neither the selective thromboxane A2 synthetase inhibitor furegrelate sodium, the stable epoprostenol (PGI2) analog ciprostene calcium, nor the selective 5-lipoxygenase inhibitor piriprost potassium caused any therapeutic effect. The highest dose of the TXA2 synthetase inhibitor (30 mg/kg IV) actually had a statistically significant detrimental action that appeared to be due to an increase in posttraumatic cerebral hemorrhage. The possible mechanisms of the beneficial effect of ibuprofen in acute head injury are discussed in relation to an attenuation of the synthesis of vasoactive arachidonic acid metabolites (e.g., prostaglandin F2 alpha, thromboxane A2) and oxygen-free radical-induced lipid peroxidation.

Animals↗
PubMed2006

Complete neurological recovery following delayed initiation of hypothermia in a victim of warm water near-drowning.

Induced hypothermia has been demonstrated to improve outcome following cardiac arrest and is now widely endorsed. However, the optimal method of cooling and the identification of patients most likely to benefit from this therapy remains to be determined. We report a patient in whom there was a long delay in return of spontaneous circulation (at least 45 min) and the initiation of induced hypothermia (12 h) who made an almost complete neurological recovery following cardiac arrest from warm-water near-drowning.

Electroencephalography↗
PubMed1985

Effect of TRH analogs on neurologic recovery after experimental spinal trauma.

Effects of two stable TRH analogs were compared after experimental spinal trauma in cats. CG3509, which has a substitution at the amino-terminus of the peptide, improved neurologic recovery; MK771, which has modifications at both ends of the tripeptide, was ineffective. These findings indicate that TRH analogs may be of use in spinal cord injury, and suggest that the C-terminal amino acid may be critical for the beneficial effects of TRH or TRH-analogs in CNS injury.

Animals↗
PubMed1987

Intramedullary spinal cord metastasis in Hodgkin's disease. Rapid diagnosis and treatment resulting in neurologic recovery.

Intramedullary spinal cord metastases are uncommon in Hodgkin's disease and have a poor prognosis. This prognosis reflects the refractory or widely disseminated status of the disease at the time of development of neurological symptoms and difficulties in diagnosis. Computerized tomography and magnetic resonance imaging have enabled more rapid and specific diagnosis of spinal cord diseases. The authors report a patient who presented with Brown-Sequard syndrome due to intramedullary spinal cord infiltration from Hodgkin's disease. This patient was diagnosed promptly and with rapid initiation of radiation and chemotherapy, she has had neurologic recovery.

Adult↗