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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This case report intends to focus attention on hemodynamic TIAs as cause of repetitive involuntary movements (RIMs) as differential diagnosis of simple partial motor seizures. We report two patients with episodic unilateral limb shaking lasting up to several minutes and which could be triggered by orthostasis, heat or physical exertion. Repeated EEG recordings revealed no epileptic discharges. In both patients, duplex ultrasonography revealed an occlusion of the internal carotid artery (ICA) contralateral to the side of the RIMs. Blood flow velocities in the middle cerebral artery ipsilateral to ICA occlusion were reduced and vasomotor reactivity to hypercapnia was absent. After elevation of blood pressure both patients became asymptomatic. We suggest that in patients with episodes of RIMs, Doppler sonography and tests of cerebral vascular reserve capacity should be performed to search for a hemodynamic origin of these symptoms.
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PMID:[Hemodynamically-induced transitory ischemic attacks. A differential focal motor seizures diagnosis?]. 983 81

Head injuries in adolescents, which often result from motor vehicle accidents, sports injuries, falls, burns, or trauma due to violence, may range from mild to severe to fatal. One of the most useful initial scoring systems is the Glasgow Coma Scale. Proper care of the injured adolescent begins at the scene of the incident, with an emphasis on management of the airways, breathing, and circulation (the ABCs) and prevention of secondary injury, which may result from hypoxia, hypercarbia, rapid swings in blood pressure, hypovolemia, seizures, and poor or improper immobilization. Monitoring and management of intracranial pressure become a priority on arrival at the emergency department. Imaging techniques, such as CT scan, may be necessary. Injuries to the neck (cervical spine), which may result in quadriplegia, should be suspected in the presence of neurologic deficits.
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PMID:Adolescent Head and Neck Trauma. 1035 4

Idiopathic congenital central alveolar hypoventilation syndrome, otherwise known as Ondine's curse, is a rare neuropathologic syndrome characterized by an inadequate respiratory drive with hypoventilation and periods of prolonged apnea resulting in hypercarbia and hypoxemia. Although no definite pathologic abnormality has been identified to account for the disorder, it is thought to represent a primary defect related to altered function of central chemoreceptors resulting in defective control of minute ventilation. Associated problems related to neural crest cell migration, including neuroblastoma formation and Hirschsprung's disease, suggest that the primary defect is defective neural crest cell migration and function. Problems that may impact on perioperative care include the defective central control of ventilation and defective control of upper respiratory musculature, which may lead to upper airway obstruction. Although many patients will have previously undergone tracheostomy and chronic mechanical ventilation, problems in other organ systems can impact on perioperative care. Cardiovascular issues include the possible presence of cor pulmonale and autonomic nervous system dysfunction. Central nervous system issues include the frequent occurrence of seizures and mental retardation. The preoperative work-up, premedication, and the intraoperative/postoperative care and monitoring of these patients is reviewed.
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PMID:Anesthetic care for the child with congenital central alveolar hypoventilation syndrome (Ondine's curse). 1052 17

Advanced prehospital emergency medical care of patients with a severe head injury must essentially focus on the impact of secondary cerebral insults of systemic origin on the outcome. The first objective of prehospital care is to prevent hypoxaemia and hypercapnia. Therefore, all patients with a Glasgow Coma Scale score equal to or lower than 8 must be treated with endotracheal intubation and controlled ventilation under continuous monitoring of SpO2 and PETCO2. Treatment is similar in head-injured patients with significant deterioration of consciousness level, seizures, respiratory distress, or severe facial and thoracoabdominal injuries. The endotracheal tube is inserted by the orotracheal route under direct laryngoscopy, after a rapid induction sequence of anaesthesia and immobilization of the cervical spine in neutral position. For the induction of anaesthesia in these high-risk patients (full stomach, unknown medical history, deteriorated haemodynamic status), etomidate and suxamethonium are the preferred agents. Sedation is maintained with an hypnoticopioid association (fentanyl). Simultaneously, the main goal is the maintenance of an optimal cerebral perfusion pressure, as arterial hypotension severely worsens cerebral ischaemia. Volume loading is accomplished with 0.9% saline and hydroxyethyl starch.
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PMID:[Prehospital management of patients with severe head injuries]. 1083 14

Slow shifts in the human scalp-recorded EEG, including those related to changes in brain CO(2) levels, have been generally assumed to result from changes in the level of tonic excitation of apical dendrites of cortical pyramidal neurons. We readdressed this issue using DC-EEG shifts elicited in healthy adult subjects by hypo- or hypercapnia. A 3-min period of hyperventilation resulted in a prompt negative shift with a rate of up to 10 microV/s at the vertex (Cz) and an extremely steep dependence (up to 100 microV/mmHg) on the end-tidal Pco(2). This shift had a maximum of up to -2 mV at Cz versus the temporal derivations (T3/T4). Hyperventilation-like breathing of 5% CO(2)-95% O(2), which does not lead to a significant hypocapnia, resulted in a near-complete block of the negative DC shift at Cz. Hypoventilation, or breathing 5% CO(2) in air at normal respiratory rate, induced a positive shift. The high amplitude of the voltage gradients on the scalp induced by hyperventilation is not consistent with a neuronal origin. Instead, the present data suggest that they are generated by extracortical volume currents driven by a Pco(2)-dependent potential difference across epithelia separating the cerebrospinal fluid and blood. Since changes in respiratory patterns and, hence, in the level of brain Pco(2), are likely to occur under a number of experimental conditions in which slow EEG responses have been reported (e.g., attention shifts, preparatory states, epileptic seizures, and hypoxic episodes), the present results call for a thorough reexamination of the mechanisms underlying scalp-recorded DC-EEG responses.
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PMID:Millivolt-scale DC shifts in the human scalp EEG: evidence for a nonneuronal generator. 1261 37

In newborn pigs, the mechanism of seizure-induced cerebral hyperemia involves carbon monoxide (CO), the vasodilator product of heme catabolism by heme oxygenase (HO). We hypothesized that seizures cause cerebral vascular dysfunction when HO activity is inhibited. With the use of cranial window techniques, we examined cerebral vascular responses to endothelium-dependent (hypercapnia and bradykinin) and endothelium-independent (isoproterenol and sodium nitroprusside) dilators during the recovery from bicuculline-induced seizures in saline controls and in animals pretreated with a HO inhibitor, tin protoporphyrin (SnPP). SnPP (3 mg/kg iv) blocked dilation to heme and reduced the CO level in cortical periarachnoid cerebrospinal fluid, indicating HO inhibition in the cerebral microcirculation. In saline control piglets, seizures increased the CO level, which correlated with the time-dependent cerebral vasodilation; during the recovery (2 h after seizure induction), responses to all vasodilators were preserved. In SnPP-treated animals, cerebral vasodilation and the CO responses to seizures were greatly reduced, and cerebral vascular reactivity was severely impaired during the recovery. These findings suggest that HO in the cerebral microcirculation is rapidly activated during seizures and provides endogenous protection against seizure-induced vascular injury.
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PMID:Endogenous heme oxygenase prevents impairment of cerebral vascular functions caused by seizures. 1291 92

Secondary brain injury is a complicated, multifactorial process that results from hypoxemia, hypercapnia or hypocapnia, and increased ICP. Implementation of a traumatic brain injury protocol for patients with head injury including hemodynamic management, pulmonary care, maintenance of body temperature, control of the environment, positioning of patients, and seizure prophylaxis provides critical care nurses a proactive means to prevent or minimize the development of secondary brain injury in the emergency department.
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PMID:Nursing role on preventing secondary brain injury. 1758 40

We studied the mechanisms underlying CO(2)-dependent DC potential shifts, using epicranial, epidural, epicortical, intraventricular, and intraparenchymal (intraneuronal, intraglial, and field) recordings in ketamine-xylazine-anesthetized cats. DC shifts were elicited by changes in artificial ventilation, causing end-tidal CO(2) variations within a 2-5% range. Hypercapnia was consistently associated with negative scalp DC shifts (average shift -284.4 microV/CO(2)%, range -216 to -324 microV/CO(2)%), whereas hypocapnia induced positive scalp DC shifts (average shift 307.8 microV/CO(2)%, range 234 to 342 microV/CO(2)%) in all electrodes referenced versus the nasium bone. The former condition markedly increased intracranial pressure (ICP), whereas the latter only slightly reduced ICP. Breakdown of the blood-brain barrier (BBB) resulted in a positive DC shift and drastically reduced subsequent DC responses to hypo-/hypercapnia. Thiopental and isoflurane also elicited a dose-dependent positive DC shift and, at higher doses, hypo-/hypercapnia responses displayed reverted polarity. As to the possible implication of neurons in the production of DC shifts, no polarity reversal was recorded between scalp, various intracortical layers, and deep brain structures. Moreover, the membrane potential of neurons and glia did not show either significant or systematic variations in association with the scalp-recorded CO(2)-dependent DC shifts. Pathological activities of neurons during spike-wave seizures produced DC shifts of significantly smaller amplitude than those generated by hyper-/hypocapnia. DC shifts were still elicited when neuronal circuits were silent during anesthesia-induced burst-suppression patterns. We suggest that potentials generated by the BBB are the major source of epicortical/cranial DC shifts recorded under conditions affecting brain pH and/or cerebral blood flow.
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PMID:Nonneuronal origin of CO2-related DC EEG shifts: an in vivo study in the cat. 1505 89

The extended postictal state is characterized by neurological problems in patients. Inadequate blood supply to the brain and impaired cerebral autoregulation may contribute to seizure-induced neuronal damage. Recent evidence in newborn pigs indicates that activation of the antioxidative enzyme heme oxygenase (HO) at the onset of seizures is necessary for increased cerebral blood flow during the ictal episode and for normal cerebral vascular functioning during the immediate postictal period. We hypothesized that seizures cause prolonged postictal cerebral vascular dysfunction that can be accentuated by HO inhibition and rescued by HO overexpression. Cerebral vascular responses to endothelium-dependent (hypercapnia, bradykinin) and -independent (isoproterenol, sodium nitroprusside) stimuli were assessed 48 h after bicuculline-induced seizures in: 1) saline-control newborn piglets, 2) HO-inhibited animals (HO was inhibited by tin protoporphyrin, SnPP, 3 mg/kg iv), and 3) HO-overexpressing piglets (HO-1 was upregulated by cobalt protoporphyrin, CoPP, 50 mg/kg ip). Extended alterations of HO expression in cerebral microvessels were confirmed by measuring CO production and inducible HO (HO-1) and constitutive HO (HO-2) proteins. Our data provide evidence that seizures cause a severe, sustained, postictal cerebral vascular dysfunction as reflected by impaired vascular reactivity to physiologically relevant dilators. During the delayed postictal state, vascular reactivity to all dilator stimuli was reduced in saline control and, to a greater extent, in HO-inhibited animals. In CoPP-treated piglets, no reduction in postictal cerebral vascular reactivity was observed. These findings may indicate that CoPP prevents postictal cerebral vascular dysfunction by upregulating HO-1, a finding that might have implications for preventing postictal neurological complications.
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PMID:Epileptic seizures cause extended postictal cerebral vascular dysfunction that is prevented by HO-1 overexpression. 1568 2

Cardiac arrest is a common disease in the United States, and many patients will die as a result of the neurological damage suffered during the anoxic period, or will live in a neurologically debilitated state. When cardiopulmonary-cerebral resuscitation results in the return of spontaneous circulation, intensive care is required to optimize neurological recovery. Such "brain-oriented" therapies include routine care, such as positioning and maintenance of volume status; optimization of cerebral perfusion, with the use of vasopressors if needed; management of increased intracranial pressure with agents such as hypertonic saline; assuring adequate oxygenation and avoiding hypercapnia; aggressive fever control; intensive glucose control, with the use of an insulin drip if needed; and management of seizures if they occur. To date, no neuroprotectant medications have been shown to improve neurological outcome. Induced moderate therapeutic hypothermia is utilized as a neuroprotective maneuver. Future treatment options and advanced monitoring techniques are also discussed. Further study to optimize neuroprotective strategies when treating patients who survive cardiac arrest is needed.
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PMID:Postresuscitative intensive care: neuroprotective strategies after cardiac arrest. 1696 40


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