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Neurologic recovery occurred in a 3-year-old patient following immersion hypothermia and prolonged cardiopulmonary resuscitation. Recognition of hypothermia in the near-drowning victim is imperative for appropriate resuscitative efforts. Intensive care monitoring (intracranial pressure, pulmonary artery catheterization) facilitates patient management and optimum neurologic recovery.
A retrospective study was conducted to evaluate the outcome of near-drowning patients admitted to the intensive care unit (ICU) comparing seawater and freshwater drownings. A chart review was used to identify near-drowning patients admitted to ICU from 1 April 1989 to 1 May 1996 for biodata, physiological data and outcome. Seventeen near-drowning patients were admitted to ICU over a period of nearly 7 years. There were 3 deaths (17.6%) and 8 patients (47%) required cardiopulmonary resuscitation. Freshwater near-drowning occurred in 8 patients and saltwater near-drowning occurred in 9 patients. Nearly all (94%) the patients had a PaO2/FiO2 ratio < 300 mm Hg. Pulmonary oedema was present on the chest radiographs of all patients. Mechanical ventilation was required for 8 patients (47%), and nearly all (94%) received prophylactic antibiotics. None of the patients developed pneumonia. Serum electrolytes and haemoglobin concentration were not grossly abnormal although, those with saltwater near-drowning had a significantly higher level of haemoglobin, sodium and urea compared to those with freshwater near-drowning. Patients that survived to hospital discharge had full neurological recovery and stayed an average of 4.5 days. We concluded that near-drowning victims that survive to be admitted to ICU have significant oxygenation defect with nearly half requiring ventilatory support. Mortality is appreciable, but those that survive to hospital discharge had full neurological recovery.
We studied cardiovascular changes and neurologic outcome at 72 h in 42 healthy dogs after normothermic ventricular fibrillation cardiac arrest (no blood flow) of 7.5, 10, or 12.5 min duration, reversed by standard external cardiopulmonary resuscitation (CPR) (< or = 10 min) and followed by controlled ventilation to 20 h and intensive care to 72 h. We found no difference in resuscitability, mortality, neurologic deficit scores, or overall performance categories between the three insult groups. There was no major pulmonary dysfunction. During controlled normotension post-CPR, all dogs presented a transient reduction in cardiac output. In the 12.5-min cardiac arrest group the decrease in cardiac output persisted beyond 12 h post-CPR (P < 0.01) and was associated with more severe arrhythmias (P < 0.05) and worse morphologic myocardial damage (P < 0.01). Both cardiac and neurologic malfunction at 72 h correlated with arrest time. Only cardiac malfunction correlated with CPR time. Neurologic recovery correlated with mild (inadvertent) pre-arrest hypothermia, diastolic arterial pressure during CPR and absence of cardiovascular impairment at 12 h post-CPR. We conclude that prolonged cardiac arrest in previously healthy dogs is followed by persistent cardiovascular derangements that correlate with impaired neurologic recovery.
PURPOSE: To describe MR features of spinal trauma and assess the value of MR imaging in the prognosis. MATERIAL AND METHODS: Retrospective confrontation between initial and follow up MRI findings and clinical features in 7 young patients with spinal cord injury. RESULTS: Five lesions were due to motor vehicle accidents and 2 lesions were secondary to falls. Five patients had multiple associated injuries, 1 patient had associated spinal vertebrae injury, the last had Spinal Cord injury Without Radiological Abnormalities (SCIWRA). A motor deficit was noted in 5 cases of paraplegia, a case of monoplegia and a case of tetraparesia. The initial MRI showed in 3 cases intramedullary hemorrhage, cord edema in 2 cases and spinal cord compression and contusion in 1 case. Initial MRI was not done in the remaining case. No cord transection was noted. Outcomes were marked by lack of significant neurological recovery with complications due to bed confinement in 5 cases, and complete neurolgical recovery in two cases. In follow up, MR findings included post traumatic cystic lesion (2 cases), "ad integrum" restitution (1 case), segmental atrophy with gliosis (2 cases) and myelomalacia in the 2 other cases. CONCLUSION: MR may offer new possibilities in establishing the prognosis for neurological recovery. Our study demonstrated a good correlation between imaging findings, clinical features and outcomes. A hemorrhagic contusion in the acute stage indicated a poor prognosis while a focal hyperintense area on T2-weighted images may resolve.
A 45-year-old-woman was presented with fever, microangiopathic hemolytic anemia, thrombocytopenia, purpura, and mental status changes. She was diagnosed as having thrombotic thrombocytopenic purpura (TPP). She was treated with daily plasma exchange and antiplatelet drugs, steroids, and vincristine. This patient had a remarkable course with 18 days of coma on full therapy followed by essentially complete recovery coincident with an increase of the plasma exchange dose to two plasma volumes processed per procedure. The patient has remained well with discontinuation of plasma exchange. We conclude that prolonged coma without evidence of major central nervous system structural lesions in TTP should be treated vigorously and continuously with plasma exchange.
We have recently demonstrated marked neuroprotective efficacy of a combination therapy with magnesium (calcium- and glutamate-antagonist), tirilazad (antioxidant) and mild hypothermia (MTH) in a rat model of transient focal cerebral ischemia. In the present study, we investigated MTH under conditions of permanent focal cerebral ischemia. In part I, 20 Sprague-Dawley rats were subjected to 6 h of permanent, laser-Doppler flowmetry (LDF) controlled middle cerebral artery occlusion (MCAO). Drugs were administered 30 min before and 1 h after MCAO. Hypothermia (33 degrees C) was maintained for 2 h. Infarct size was planimetrically determined after 6 h. In part II, 29 rats were assigned to the same treatment arms and subjected to 7 days of permanent MCAO. Neurological deficits and body weight were assessed daily. Infarct size was determined on day 7. In part I, MTH significantly reduced infarct formation by 52% after 6 h. In part II, high mortality within the first 3 days was observed in both groups. Treated animals showed a significantly better postoperative weight gain on day 7 and neurological recovery on days 6 and 7 compared to controls without significant differences in infarct volume. MTH seems to exert its neuroprotective properties even in a setting of permanent cerebral ischemia. High mortality and absence of infarct reduction after 7 days might be due to model limitations. Neurological recovery, the most important clinical outcome parameter, is significantly improved in 7-day survivors. Significant neuroprotection under conditions of permanent ischemia and former promising results in transient ischemia justify further investigations of MTH.
Cryosurgery has many advantages in the treatment of musculoskeletal tumors, but complications can occur, with injuries to the peripheral nerves. Cryoprotectants such as dimethylsulfoxide (DMSO) and glycerol enhance the in vitro survival of cultured Schwann cells, but they have not been studied in vivo. In vitro, 10 percent DMSO provided the maximal survival after freezing to -80 degrees C. The neurologic recovery of a peripheral nerve, following cryoinjury and using liquid nitrogen, was evaluated both with and without pretreatment of the nerve with 10 percent DMSO. There were three experimental groups: 1) one sham operation; 2) with freezing of the sciatic nerve; and 3) with freezing of the sciatic nerve after treatment with DMSO. Gait analyses (sciatic function index, SFI), muscle weights, and histologic evaluations were performed in order to follow the neurologic recovery over a ten-week period. The freezing-only group and the sham-operated control had an excellent functional recovery in terms of the SFI following surgery (-4.2 percent +/- 4.0 percent and -2.4 percent +/- 5.7 percent, respectively), in contrast to the freezing group with DMSO (-34.1 percent +/- 5.5 percent, p less than .01). The average tibialis anterior muscle weight, reported as the ratio of the operated to the unoperated limb (88.2 percent +/- 1.0 percent) in the freezing-only group, was greater than the average for the freezing-with-DMSO-treated group (70.6 percent +/- 3.9 percent, p less than .01). Cryoprotectants are routinely used to optimize the survival of cells in tissue culture. However, DMSO not only failed to protect peripheral nerves from cryoinjury, but it also inhibited functional recovery.
AIM: To investigate the neuroprotective effect of resveratrol in an experimental spinal cord injury (SCI) model in rats. METHODS: Male Wistar albino rats weighing 200-250 g were randomized into six groups. Weight-drop trauma was performed for SCI. Group 1 underwent laminectomy alone. Group 2 underwent laminectomy followed by SCI. Groups 3, 4, 5, and 6 underwent laminectomy followed by SCI and received resveratrol (100 mg/kg), methylprednisolone (MP) (30 mg/kg), resveratrol (100 mg/kg) plus MP (30 mg/kg), and ethanol (2%), respectively. The rats were divided into two subgroups for biochemical analysis (killed at 24 h after surgery) and for neurobehavioral and histopathological evaluation (killed at 6 weeks after surgery). Posttraumatic neurological recovery after surgery was recorded weekly. RESULTS: Groups 3 and 5 revealed significantly lower malon-dialdehyde, nitric oxide, xanthine oxidase, and higher glutathione levels than group 4 (P<0.05). Neurological recovery rates were significantly better in groups 3 and 5 than group 4 (P<0.05). When spinal trauma size ratios were compared, there was no significant difference between treatment groups. CONCLUSION: Resveratrol treatment revealed better biochemical recovery in the acute stage of trauma than MP treatment. Although resveratrol and combined treatment revealed better neurobehavioral recovery than MP treatment; resveratrol, MP, and combined treatment modalities improved histopathological recovery at the same level in the final stage of the experiment. Future studies involving different doses of resveratrol and different doses combinations with MP could promise better results as each drug has a different anti-oxidative mechanism of action.
The pathogenesis and clinical course of traumatic cerebral vasospasm (TCV) are not yet fully understood. We report a case of delayed symptomatic TCV exaggerated by hyponatremia in spite of minor subarachnoid hemorrhage. A 77-year-old woman was admitted to our hospital with multiple injury caused by a traffic accident. Glasgow coma scale on admission was 8, and CT scan revealed right temporal lobe contusion, thin sub-arachnoid hemorrhage in the right sylvian cistern and right temporal bone fracture. The patient's consciousness level and CT findings improved gradually, but on the 11th day, she suddenly fell into a comatose state. No apparent change was observed on the CT scan, but her serum sodium level was markedly low (113 mEq/L). Under the suspicion of hyponatremia induced consciousness disturbance, sodium replacement therapy was commenced. She showed transient neurological recovery, but on day 13, worsening of left hemiparesis and a new low density area on CT were observed. Vasospasms of the right M2 proximal portion were confirmed by cerebral angiogram, so we performed intraarterial papaverine infusion leading to good extension of spastic vessels, but regrettably, there was no neurological recovery. In general, subarachnoid blood plays an important role in the delayed development of cerebral vasospasm, following not only aneurysmal rupture but also head injury. TCV tends to pass subclinically, but secondary water and electrolyte imbalance may unexpectedly cause TCV to manifest itself clinically. We can confirm that with this patient management of electrolyte balance following head injury was the most important strategy to avoid symptomatic TCV.
Oxygen radical-mediated lipid peroxidation appears to be a critical factor in posttraumatic neuronal degeneration. Thus, numerous studies have evaluated the neuroprotective efficacy of pharmacologic agents with lipid antioxidant activity in models of spinal cord and brain injury. Intensive pretreatment of animals with the endogenous lipid peroxyl radical scavenger alpha tocopherol (i.e., vitamin E) has been shown to decrease posttraumatic spinal cord ischemia and to enhance chronic neurologic recovery. However, the slow CNS tissue uptake of vitamin E requires chronic dosing, making it an impractical agent for the treatment of acute neural injury. The glucocorticoid steroid methylprednisolone has been shown to possess significant antioxidant efficacy and, when administered to animals or humans in antioxidant dosages, improves chronic neurologic recovery after spinal cord injury. This activity of methylprednisolone is independent of the steroid's glucocorticoid receptor-mediated actions. Novel antioxidant 21-aminosteroids have been developed that are devoid of glucocorticoid activity but have greater antioxidant efficacy than methylprednisolone. One of these, U74006F or tirilazed mesylate, has been shown to be effective in animal models of brain and spinal cord injury and is currently undergoing phase II clinical trials. Compounds that combine the amino functionality of the 21-aminosteroids with the peroxyl radical scavenging chromanol portion of vitamin E (i.e., 2-methylaminochromans) have also recently shown promise as neuroprotective agents. The consistent benefit afforded by antioxidant compounds adds further support to the concept that lipid peroxidation is an important therapeutic target for acute pharmacologic neuroprotection.
Two cases of neurological dysfunction are presented. Neurological deficits after recovery from anaesthesia are unusual in young women perioperatively. In the first case, a 39-yr-old woman presented at 36-wk gestation with antepartum haemorrhage and in labour. Pregnancy had been complicated by pre-eclampsia and she underwent emergency Caesarean section under general anaesthesia without complication. The trachea was extubated when she was awake but almost immediately she became hypertensive, obtunded and reintubation was required. Her pupils became fixed and dilated but the Computerised Axial Tomogram (CT) was normal. A coagulopathy was evident. She made a full neurological recovery within 24 hr. On the same day, a previously healthy 41-yr-old woman who had undergone uneventful surgery for uterine prolapse 24 hr previously developed headache, nausea and over the next four hours signs of progressive brainstem ischaemia. The CT scan showed oedema of the mid- and hindbrain. Brainstem death was confirmed 12 hr later and the post-mortem revealed acute dissection of the vertebral artery secondary to cystic medial necrosis. Such dramatic neurological sequelae are rare but the importance of identifying "at risk" groups is underlined as is early recognition of neurological injury postoperatively.
PURPOSE: This study was undertaken to evaluate whether neurologic outcome after aortic cross-clamping in rabbits could be improved with perioperative infusion of the hydroxyl radical scavenger dimethylthiourea and, if so, to determine whether it is effective during the period of ischemia, reperfusion, or both. METHODS: In 41 New Zealand White rabbits, a snare occlusion device was placed at operation around the infrarenal aorta and tunneled into a subcutaneous position. Animals were then allowed to recover and, 48 hours later, randomized into four groups. In each group, the infrarenal aorta was occluded by tightening the snare in the awake animal. In groups 1, 2, and 3, cross-clamp time was 21 minutes. Group 1 (control) animals received saline solution, whereas group 2 (preclamp 21) received dimethylthiourea 750 mg/kg intravenously just before aortic clamping. In group 3 (prerep 21), dimethylthiourea was given just before reperfusion. Group 4 received dimethylthiourea before clamping, with cross-clamp time extended to 31 minutes. A second dose of saline solution or dimethylthiourea was given 12 hours after clamping in controls and the three treatment groups, respectively. Animals were observed for 5 days, and final neurologic recovery was graded by an independent observer. Animals were then killed, and their spinal cords were removed for histologic examination. RESULTS: Complete paraplegia and marked histologic spinal cord injury at 5 days were seen in 91% (10/11) of group 1 (control) animals, whereas all animals in group 2 (preclamp 21) showed neurologic recovery (p < 0.0001). In group 3 (prerep 21), the final paraplegia rate was 50% (5 of 10), in group 4 (preclamp 31), 100% (10 of 10). CONCLUSIONS: Our results suggest that hydroxyl radicals play an important role in ischemia-reperfusion injury of the spinal cord and that treatment with dimethylthiourea can prevent paraplegia after 21 minutes of aortic cross-clamping in rabbits.
Oxygen radical-mediated lipid peroxidation (LP) has been suggested increasingly to be an important factor in posttraumatic neuronal degeneration. Thus, numerous studies have evaluated the neuroprotective efficacy of pharmacological agents with lipid antioxidant activity in models of spinal cord and brain injury. Intensive pretreatment of animals with the endogenous lipid peroxyl radical scavenger vitamin E (i.e., alpha-tocopherol) has been shown to decrease posttraumatic spinal cord ischemia and to enhance chronic neurological recovery. However, the slow CNS tissue uptake of vitamin E requires chronic dosing, making it an impractical agent for treatment of acute neural injury. The glucocorticoid steroid, methyl-prednisolone (MP), has been shown to possess significant antioxidant efficacy and, when administered to animals or humans in antioxidant doses, improves chronic neurological recovery after spinal cord injury. This activity of MP is independent of the steroid's glucocorticoid receptor-mediated actions, as evidenced by the efficacy of the novel antioxidant 21-aminosteroids, which are devoid of glucocorticoid activity but have greater antioxidant efficacy than MP. One of these, tirilazad mesylate (U-74006F), has been shown to be effective in animal models of brain and spinal cord injury and is currently the subject of phase II clinical trials. Recently, compounds that combine the amino functionality of the 21-amino-steroids with the peroxyl radical scavenging chromanol portion of vitamin E (i.e., 2-methylaminochromans) also have shown promise as neuroprotective agents. The consistent benefit afforded by antioxidant compounds further supports the concept that LP is an important therapeutic target for acute pharmacological neuroprotection.
A 15-year-old boy suffered from progressive bilateral optic neuropathy of acute onset at the age of 10 years. Subsequently he developed spastic paraparesis and a predominantly motor type neuro-axonal neuropathy in all limbs. The basic error has been elucidated to be due to an unusual biotinidase Km variant with biphasic enzyme kinetics causing systemic biotin depletion and consequent multiple biotin-dependent carboxylase deficiency. After daily oral substitution with 10 mg biotin metabolic derangements subsided rapidly. Follow-up studies over one year after substitution with biotin demonstrated remarkable recovery from part of the previously present neuro-ophthalmological, motor and cognitive deficits. The previously extinguished flash-evoked visual potentials now showed clear responses after six months of substitution with biotin. In contrast with reports in literature, these findings indicated that neurological damage associated with biotinidase deficiency, rather than being permanent, is to some extent reversible.
The authors reviewed 85 patients who had undergone anterior decompression and cervical fusion for myeloradiculopathy due to ossification of the posterior longitudinal ligament. There were 72 males and 13 females; the average follow up was for 8.3 years. Sixteen patients (group I) underwent one vertebra subtotal spondylectomy with fusion, 58 (group II) two vertebra subtotal spondylectomy, and 11 (group III) three vertebra subtotal spondylectomy. Neurological recovery was assessed on the grading system of the Japanese Orthopaedic Association. The patients in group I had an average improvement of 75%, in group II 72% and in group III 23%. The severity of compromise of the spinal cord did not affect the postoperative improvement. Duration of disease, previous injury and advanced neurological symptoms all affected neurological recovery. Spondylectomy of at most two vertebrae, with fusion, is recommended for ossification of the posterior longitudinal ligament. If there is more extensive involvement laminoplasty may be indicated.
An experimental model of cat spinal injury was used to investigate the hypotheses that endorphins are involved in the pathophysiology of spinal cord injury and that the opiate antagonist naloxone, by blocking the effects of endorphins, may improve physiological and neurological recovery. Experimental trauma to the cervical spine caused a reduction in blood pressure and spinal cord blood flow (SCBF) associated with increased plasma levels of beta-endorphin-like immunoreactivity; both blood pressure and SCBF were significantly improved by naloxone treatment. Naloxone-treated animals also showed less prominent spinal cord abnormalities and significantly improved neurological recovery compared with saline controls. Moreover, both the pathological and clinical findings correlated significantly with the blood pressure changes following treatment. The data support a pathophysiological role for endorphins in experimental spinal cord injury and suggest that opiate antagonists might improve the treatment of spinal trauma in humans.
BACKGROUND: We studied the incidence and clinical significance of early post-traumatic seizures after severe closed head injury. METHODS: This prospective study is based on clinical observation of 3340 adult patients with severe closed head injuries, each of them having a Glasgow Coma Scale (GCS) 3 to 8 after trauma. Anticonvulsant agents were not given to these patients unless there was evidence of seizure. RESULTS: One hundred and twenty-one patients (3.6%) experienced seizures within 1 week after head injury; 42 of these (1.26% of the series) had seizures within 24 hours after trauma. The incidence of intracerebral parenchymal damage was found to be higher among those patients who developed seizures in the first week (66.1%) than in those who did not (62.7%). However this result did not reach statistical significance. The patients with early seizures had a lower mortality rate (p < 0.01). In patients who survived from the initial injury, the occurrence of early post-traumatic seizures did not appear to influence the neurological recovery at 6 months after injury. CONCLUSION: Presence of intracerebral parenchymal damage on CT scan after severe closed head injury does not increase the risk of early post-traumatic seizures. With proper treatment, patients presenting with early seizures may have a lower mortality rate. However, the occurrence of early seizures does not influence the neurological recovery in patients who survive the initial severe closed head injury.
The effect of anesthesia upon the functional outcome after experimental spinal cord injury (SCI) was studied in 221 rats subjected to graded weight drop contusion in the thoracic cord. Neurologic function was assessed in a blinded fashion for one week after injury using a modification of the method of Tarlov. The post-mortem concentrations of serotonin and its metabolite were measured in injured and surrounding spinal tissues in a subset of animals in order to estimate the survival of descending long-tract axons. In initial studies using non-ventilated animals where body temperature was not controlled (n = 130), halothane anesthesia was associated with significantly better neurologic scores at all levels of injury (50, 100 and 250 g.cm) in comparison to pentobarbital. In a second experiment under these conditions (n = 53) the effect of halothane was observed after a 50 g.cm injury in comparison to both pentobarbital and nitrous oxide. Improved neurologic recovery was accompanied by the preservation of normal serotonin and metabolite concentrations in spinal tissue caudal to the site of injury. These values did not differ from those measured in sham-operated animals. Separate experiments (n = 12) revealed halothane's preservation of somatosensory-evoked responses during the early postinjury period in animals showing improved neurologic recovery. Subsequent experiments (n = 12) were performed to assess the effect of oxygen supplementation and the control of rectal temperature and a separate series of acute experiments (n = 14) examined arterial blood pressure responses to injury in halothane- and pentobarbital-anesthetized animals.(ABSTRACT TRUNCATED AT 250 WORDS)