Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085631 (agitation)
 12,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The most venomous scorpion species are Buthotus tamulus of India, the Leiurus quinquestriatus and Androctonus crassicauda of North Africa and the Middle East, the Tityus serrulatus of Brazil, and the Centruroides suffussus of Mexico. The severity of scorpion envenomation varies with the scorpion's species, age, and size, and is much greater in children. Systemic intoxication reflects the overstimulation of the CNS, the sympathetic and parasympathetic nervous system. Severity ranges from local pain and paresthesia to fatal cardiotoxicity and encephalopathy. Symptoms include: agitation, tachycardia, vomiting, abdominal pain, salivation, diaphoresis, dehydration, muscle rigidity and twitching, tremor, seizures, coma, pupillary changes, hyperthermia, tachyarrythmias and occasionally bradyarrhythmias, hypertension, and less often hypotension, cardiac failure, and priapism in males. Laboratory abnormalities include: hyperglycemia, leucocytosis, transient elevation of cardiac and pancreatic enzymes, ischemic changes in the ECG, and evidence of cardiac dysfunction on echocardiography. The principles of management are: observation, cardiac monitoring, supportive treatment with intravenous fluids and electrolytes, and a meticulous use of cardiovascular agents: vasodilators, adrenergic antagonists, or calcium channel blockers in the hypertensive phase; and inotropic agents in the event of hypotension. Antiarrhythmics such as lidocaine, may be required. There is increasing evidence for the efficacy of specific antivenom. The advance in supportive care and antivenom efficacy has markedly improved the outcome of patients with scorpion envenomation.
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PMID:Clinical manifestations and management of scorpion envenomation. 1044 63

We present a 1 7-year-old female with acute extra-pyramidal parkinsonism complicating a suicidal attempt with the organophosphate insecticide chlorpyrifos, who was initially suspected to have developed severe depression or psychosis. On admission she was stupurous, with diarrhoea and massive salivation lapsing into respiratory failure and coma. Following atropine and toxogonin treatment along with mechanical ventilation she developed overt extrapyramidal parkinsonism and encephalopathy, characterized by impaired sensorium and agitation, mask facies along with a muffled voice and swallowing impairment, a resting tremor with cogwheel rigidity switching to bradykinetic choreoathetotic movements. Once a parkinsonian syndrome was diagnosed, she was given amantadine therapy with complete recovery. The patient is presently maintained on amantadine therapy; there was mild worsening of her extrapyramidal signs following unplanned discontinuation of this medication, and on follow-up assessments after 9 months she is virtually asymptomatic. A parkinsonian extrapyramidal syndrome, complicating organophosphate intoxication, should therefore also be taken into account in any patient with organophosphate poisoning, presenting with marked behavioural alterations, rigidity or akinetic mutism, and beneficial response to amantadine.
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PMID:Extra-pyramidal parkinsonism complicating organophosphate insecticide poisoning. 1176 85

To define the incidence and type of neurological complications and associated factors, we reviewed 41 consecutive patients who had 45 procedures for liver transplantation. Encephalopathy occurred after 28 procedures (62%) with immediate onset and no significant recovery before death or re-transplantation in 11 (24%), slow recovery in eight (18%) and delayed onset (1-50 days, average 11) in six (13%). Intermittent confusion and agitation with full recovery followed three (6.6%), and focal and generalized seizures followed five (11%) procedures with multifocal myoclonus in two and status epilepticus in one; isolated focal seizures followed two and myoclonus or unclassified seizures, one each. All patients with seizures had encephalopathy. Three patients had neuropathy (2 generalised and 1 focal). Other complications included headache (2), tremors (2), fatigue (2), restlessness, nervousness, transient enuresis, intermittent dizziness, critical illness myopathy and detached retina. Brain imaging showed atrophy in three (6.6%) instances, intracerebral haemorrhage in two, multiple infarctions in one, and intracerebral and subarachnoid haemorrhage with infarction in one. Cerebrospinal fluid analysis showed increased protein in three, hemorrhage in one, and no abnormality in one patient. Of 12 patients (29%) who died before discharge, five in the first and three in the second week post-transplantation, 11 (92%) had encephalopathy post-operatively. Neurological complications after transplantation were associated with increased mortality. Post-operative hypomagnesaemia was associated with the development of nervous system complications. We did not identify any clear pre-operative predictors of development of post-operative neurological complications.
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PMID:Neurological complications in liver transplantation. 1201 80

23% of all septic patients develop septic encephalopathy which is associated with an increased mortality rate. Symptoms such as agitation, confusion and disorientation ranging from stupor to coma often develop in early sepsis. Severe hypotension is significantly associated with the development of septic encephalopathy. Several other factors which may play a role are also discussed: effects of inflammatory mediators on the brain, inadequate cerebral perfusion pressure, blood-brain barrier derangements, disturbances of the cerebral microcirculation, cerebral ischemia e.g. due to hypocapnia,metabolic changes, altered amino acid levels, transmitter imbalances, liver insufficiency, multiple organ failure and infections of the CNS, respectively. Compared to patients with an isolated infection,patients in septic shock have increased levels of aromatic amino acids such as phenylalanine and tryptophan in the plasma and brain as well as decreased levels of branched chain amino acids. Patients who died had higher levels of aromatic amino acids than the survivors. The correlation between aromatic amino acids and the APACHE II score was significant. The tryptophan metabolite quinolinic acid which can be synthesized in activated macrophages could act as an excitatory transmitter on the N-methyl-D-aspartate (NMDA) -receptor. Observations from experimental models indicate that activated NMDA receptors activate the neuronal isoform of the NO-synthase and other calcium dependent enzymes. This releases free radicals which may damage the DNA and activate the nuclear enzyme Poly-ADP-ribose-synthetase (PARS), resulting in energy depletion and cell death. Sepsis is the main cause of metabolic encephalopathies in critically ill patients. The differential diagnoses include hepatic, renal,hypoxic-ischemic or cardiovascular encephalopathies as well as encephalopathies,metabolic disorders and organ dysfunctions of other origin. Therapeutic interventions are numerous,however, so far only investigated in few controlled studies. The primary therapeutic goal is to maintain an adequate perfusion pressure and to prevent hypoxia and hypocapnia. Although the infusion of branched chain amino acids is controversial, experimental investigations demonstrated improvements improvements in an animal model with septic encephalopathy. Further investigations with respect to glutamate receptor antagonists, new radical scavengers, NO- and PARS-inhibitors may show whether these substances are suitable for the prophylaxis or early therapy of septic encephalopathy.
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PMID:[Septic encephalopathy. Diagnosis und therapy]. 1275 14

We investigated the efficacy and safety of midazolam given intravenously for the treatment of status epilepticus in children. Patients received one to three bolus injections of midazolam (0.15 to 0.40 mg/kg) until seizures disappeared completely. In other patients, continuous infusion of midazolam (0.06 to 0.48 mg/kg/hr) followed a bolus of midazolam or other anti-epileptic agents. The dose was increased every 15 minutes until the seizures were brought under control. The etiology of 62 episodes of status epilepticus was epilepsy in 43, acute encephalopathy/encephalitis in 11, febrile seizures in 7 and hypoxic encephalopathy in 1. The age of the patients ranged from 0.2 to 18.4 years (average: 3.7 years). Bolus injections were administered in 53 episodes. The average loading dose was 0.35 +/- 0.22 mg/kg (range 0.15 to 0.90 mg/kg). Of the 42 episodes in which seizures disappeared, 13 required no further continuous infusions. Of the remaining 29 in which continuous infusion was done at the rate of 0.06 to 0.60 mg/kg/hr (mean 0.30 mg/kg/hr), 21 ended in cessation of the seizures. The duration of continuous infusions ranged from 4 to 288 hours (average 49.0 hours). In 6 episodes there were adverse effects:transient hypoxemia (5) and agitation during withdrawal (1). No intervention was needed except oxygenation by mask for less than 72 hours. Midazolam is effective and safe, and can be used as the first line drug in the treatment of status epilepticus in children.
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PMID:[Midazolam treatment for status epilepticus of children]. 1287 6

Delayed postanoxic encephalopathy is a rare condition in which patients appear to make a complete clinical recovery after an episode of anoxia or hypoxia but then develop a relapse characterized by apathy, confusion, agitation, and/or progressive neurologic deficits. The incidence of delayed postanoxic encephalopathy is unclear but has been reported to range from less than 1 to 28 per 1000 in patients who have suffered hypoxic or anoxic events. The exact pathogenesis remains unknown. We describe a case of an independently living 51-year-old woman admitted to an inpatient rehabilitation unit 11 days after a respiratory arrest. At admission, she exhibited cognitive and visual deficits that were relatively mild but prevented a safe return to independent living. Two days later, she developed the sudden onset and rapid worsening of parkinsonian symptoms and excruciating bilateral lower-extremity pain. The pain was intractable, and over the next 2 days she progressed to being unable to walk or perform her activities of daily living without maximum assistance. A diagnosis of delayed postanoxic encephalopathy was made, and the patient responded to a trial of carbidopa and levodopa as well as redirection of her physical and occupational therapy programs. This case illustrates the unusual presentation of delayed postanoxic encephalopathy during inpatient rehabilitation and suggests that this condition should be considered if patients who have suffered an anoxic or hypoxic event show a sudden neurologic deterioration.
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PMID:Delayed postanoxic encephalopathy: a case report and literature review. 1503 41

A 31-year-old man was transferred to our emergency room (ER) with acute onset of high-grade fever and consciousness disturbance. His consciousness at ER was severely disturbed with restlessness. No apparent focal neurological signs were seen. MRI with diffusion-weighted images (DWI) showed high signal intensities at the corpus callosum, left cerebellar hemisphere, left deep white matter and right middle cerebellar peduncle. These lesions were low signals in apparent diffusion coefficient(ADC) map, indicating cytotoxic edema. EEG showed enhanced fast waves seen in predominantly frontal regions. CSF examination was normal except elevated initial pressure of 210 mmH2O. He was treated with high dose dexamethasone and acyclovir. His consciousness and high-grade fever with systemic inflammatory responses were dramatically improved after these treatments. Subsequent data showed hyperthyroidism with anti-thyroid stimulating hormone receptor antibodies. This case was thought to be a thyrotoxic encephalopathy with beneficial response to corticosteroid therapy. Abnormalities seen in DWI and EEG were normalized ten days later.
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PMID:[Thyrotoxic encephalopathy showing reversible diffusion-weighted imaging abnormalities]. 1572 78

A frequent cause of fetal acidemia, which sometimes results in hypoxic-ischemic encephalopathy, is umbilical cord compression associated with uterine contraction. Using a sheep model of fetal acidemia, we examined the changes in electrocorticogram (ECoG), carotid artery blood flow, arterial blood pressure and fetal heart rate during cord compression. A characteristic burst of ECoG spikes emerged during cord compression at fetal arterial pH 7.18 even before the pH went down to severe fetal acidemia (less than 7.10). The administration of a neuromuscular blocking agent to the fetus did not abolish the appearance of the spikes. These results suggest that cord compression may cause abnormal brain excitement even in the absence of severe fetal acidemia and that this abnormal excitement can lead to fetal brain dysfunction, if cord compression is repeated or prolonged.
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PMID:Appearance of abnormal electrocorticogram patterns during umbilical cord compression in sheep fetus. 1634 Jan 68

In recent years, neuropsychiatric symptoms associated with Hashimoto thyroiditis have been increasingly recognized in both adult and pediatric patients. This neurologic complication has been termed "Hashimoto encephalopathy," and it can begin abruptly, in the form of seizures or agitation, with or without other neurologic complaints, or it can develop gradually, in a relapsing-remiting manner, including, among others, cognitive deterioration and psychiatric illness. The occurrence of Hashimoto encephalopathy is unrelated to the patient's thyroid function status. Although the pathogenesis of this encephalopathy is not fully understood, evidence for both autoimmune and vasculitic mechanisms exists. Owing to a low index of suspicion, this encephalopathy is very likely underdiagnosed in children. The diagnosis of Hashimoto encephalopathy is based on detecting antithyroid antibodies in these patients, although there is no correlation between antibody levels and the severity of the illness. Cerebrospinal fluid analysis, electroencephalography, and neuroimaging studies do not show consistent findings to support the diagnosis. Physicians' awareness of this complication is of great importance because most patients respond dramatically to corticosteroid therapy. Moreover, early recognition might also avoid an expensive diagnostic work-up in patients with unexplained encephalopathy (J Child Neurol 2006;21:1-5).
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PMID:Encephalopathy associated with Hashimoto thyroiditis: pediatric perspective. 1655 44

We examined the usefulness of Magnetic Resonance Imaging (MRI) test in the acute phase of carbon monoxide intoxication for forecasting delayed encephalopathy (DE). [Case 1] 26-year-old female. COHb 12%. Takotsubo (Ampulla) cardiomyopathy was supervened. Pallidal disorder was recognized in MRI test in the early stage. Although Prophylactic HBO was performed, DE began. 36 days later, disorder was recognized in large area, such as, in cerebral white matter and callosum, and abnormality was found in WMS-R and MMSE. Since HBO was performed, DE subsided. In MRI test, on the other hand, high signal range in cerebral white matter and callosum were gradually decreased and WMS-R and MMSE were improved. [Case 2] 19-year-old female. COHb 9.4%. The state was considered to be mild but pallidal disorder was found in MRI test at the beginning. DE did not start, then the part of pallidal disorder was narrowed. WMS-R and MMSE showed slightly low level. [Case 3] 19-year-old female. COHb 7.3%. The state was considered to be mild and there was no abnormal findings in MRI test in the early stage. DE did not start. [Case 4] 48-year-old male. COHb 48.9%. Rhabdomylosis was supervened, then ischemic change in a left radiate crown was recognized in the early MRI test. Since the third day, disorientation and restlessness had been developed, so that the patient was transferred to psychiatric department, though it was still difficult to distinguish the case from DE. Although the case is relatively mild, pallidal disorder is recognized in the early MRI test. Pallidal disorder alone can cause memory disorder and cognitive impairment. Even if pallidal disorder alone is recognized in the early MRI test, white matter disorder is developed with time, and then DE begins. If there are no typical carbon monoxide intoxication findings, some cases can be suspected as DE. It is useful to perform serial MRI test in order to prepare for delayed encephalopathy in carbon monoxide intoxication.
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PMID:[Can magnetic resonance imaging of the brain in the acute phase of carbon monoxide intoxication forecast delayed encephalopathy?]. 1753 62


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