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Medicina (Kaunas, Lithuania) 2008Coma is the disorder of consciousness because of the damage to diffused bilateral cerebral hemisphere cortex or reticular activating system. Coma can be caused by... (Review)
Review
Coma is the disorder of consciousness because of the damage to diffused bilateral cerebral hemisphere cortex or reticular activating system. Coma can be caused by neurogenic (head brain injury), metabolic (endogenic), and toxic (exogenic) factors. To determine the cause of metabolic and toxic coma, laboratory tests are performed; in case of neurogenic coma, the neurologic examination is essential, when five systems are evaluated: the level of consciousness (according to Glasgow Coma Scale or Full Outline of Unresponsiveness Scale), photoreaction of pupils and ophthalmoscopic examination, oculomotoric, motoric, and cardiopulmonary systems. For the treatment of coma, adequate oxygenation and correction of blood circulation disorders are important. The treatment of metabolic coma is guided by special schemes; antidotes often are needed in the treatment of toxic coma, and surgery helps if traumatic brain injury is present. The prognosis and outcomes of the comatose patient depend on the age and comorbid diseases of the patient, the underlying cause of coma, timely medical help and its quality, and intensive treatment and care of the patient in coma.
Topics: Aged; Brain Death; Coma; Confusion; Critical Care; Diagnosis, Differential; Electroencephalography; Glasgow Coma Scale; Humans; Lethargy; Magnetic Resonance Imaging; Prognosis; Sepsis; Stupor; Time Factors
PubMed: 19001840
DOI: No ID Found -
The Pan African Medical Journal 2021Vitamin B12 deficiency in early childhood is an important cause of neurodevelopmental delay and regression. Most of these cases occur in exclusively breast-fed infants... (Review)
Review
Vitamin B12 deficiency in early childhood is an important cause of neurodevelopmental delay and regression. Most of these cases occur in exclusively breast-fed infants of deficient mothers. Symptoms and signs of vitamin B12 deficiency appear between the ages of 2 to 12 months and include vomiting, lethargy, failure to thrive, hypotonia, and arrest or regression of developmental skills. Approximately one half of this cases exhibit abnormal movements, variously described as tremors, twitches, chorea, or myoclonus. Urinary concentrations of methylmalonic acid and homocysteine are characteristically elevated in vitamin B12 deficiency. Hyperglycinuria is sometimes present. The early diagnosis and treatment of vitamin B12 deficiency is crucial for significant neurological impairment and long-term prognosis. Treatment with vitamin B12 corrects these metabolic abnormalities very rapidly (within a few days). Vitamin B12 supplementation of pregnant women may prevent neurological and neuroradiological findings of the infants. Because of the importance of vitamin B12 in the development of the foetal and neonatal brain, vegetarian and vegan mothers should be aware of the severe and not fully-reversible damages caused by insufficient nutritional intake of vitamin B12 during pregnancy and lactation. Therefore, efforts should be directed to prevent its deficiency in pregnant and breastfeeding women on vegan diets and their infants. It is also important to take the nutritional history of both infants and their mothers for the early prevention and treatment. Here an interesting case of vitamin B12 deficiency in a 10-month-old boy presented with psychomotor regression, hypotonia and lethargy.
Topics: Breast Feeding; Dietary Supplements; Female; Humans; Infant; Male; Muscle Hypotonia; Pregnancy; Prenatal Care; Vitamin B 12; Vitamin B 12 Deficiency
PubMed: 34046142
DOI: 10.11604/pamj.2021.38.237.20967 -
Nature Sep 2022Infections induce a set of pleiotropic responses in animals, including anorexia, adipsia, lethargy and changes in temperature, collectively termed sickness behaviours....
Infections induce a set of pleiotropic responses in animals, including anorexia, adipsia, lethargy and changes in temperature, collectively termed sickness behaviours. Although these responses have been shown to be adaptive, the underlying neural mechanisms have not been elucidated. Here we use of a set of unbiased methodologies to show that a specific subpopulation of neurons in the brainstem can control the diverse responses to a bacterial endotoxin (lipopolysaccharide (LPS)) that potently induces sickness behaviour. Whole-brain activity mapping revealed that subsets of neurons in the nucleus of the solitary tract (NTS) and the area postrema (AP) acutely express FOS after LPS treatment, and we found that subsequent reactivation of these specific neurons in FOS (also known as TRAP2) mice replicates the behavioural and thermal component of sickness. In addition, inhibition of LPS-activated neurons diminished all of the behavioural responses to LPS. Single-nucleus RNA sequencing of the NTS-AP was used to identify LPS-activated neural populations, and we found that activation of ADCYAP1 neurons in the NTS-AP fully recapitulates the responses elicited by LPS. Furthermore, inhibition of these neurons significantly diminished the anorexia, adipsia and locomotor cessation seen after LPS injection. Together these studies map the pleiotropic effects of LPS to a neural population that is both necessary and sufficient for canonical elements of the sickness response, thus establishing a critical link between the brain and the response to infection.
Topics: Animals; Anorexia; Area Postrema; Brain Stem; Illness Behavior; Lethargy; Lipopolysaccharides; Mice; Neurons; Pituitary Adenylate Cyclase-Activating Polypeptide; Proto-Oncogene Proteins c-fos; Solitary Nucleus
PubMed: 36071158
DOI: 10.1038/s41586-022-05161-7 -
BMJ Case Reports Jan 2019A 60-year-old man with cerebral palsy and epilepsy was admitted with acute lethargy and deterioration in coordination. He was noted to be hypothermic at 35°C on...
A 60-year-old man with cerebral palsy and epilepsy was admitted with acute lethargy and deterioration in coordination. He was noted to be hypothermic at 35°C on admission. Routine work-up revealed toxic levels of phenytoin. No cause of hypothermia could be identified but as his phenytoin levels normalised, his body temperature also improved. There are three other reported cases of phenytoin- induced hypothermia in the literature. Could this be a rare cause of hypothermia?
Topics: Aftercare; Ataxia; Cytochrome P-450 CYP1A2 Inducers; Diagnosis, Differential; Humans; Hypothermia; Lethargy; Male; Middle Aged; Phenytoin; Treatment Outcome
PubMed: 30674493
DOI: 10.1136/bcr-2018-227443 -
Cancer Biology & Therapy Jan 2018Cytotoxic chemotherapy can induce a systemic inflammatory response which has been proposed to be an underlying mechanism of cancer treatment related fatigue....
Cytotoxic chemotherapy can induce a systemic inflammatory response which has been proposed to be an underlying mechanism of cancer treatment related fatigue. Dexamethasone, a synthetic glucocorticoid that has potent anti-inflammatory effects, is incorporated into chemotherapy regimens to prevent chemotherapy-induced nausea and vomiting (CINV). The purpose of this study was to determine whether by suppressing cytotoxic chemotherapy-induced inflammation, dexamethasone could ameliorate chemotherapy induced fatigue/lethargy in tumor free mice. The effect of dexamethasone (DEX) on Cytoxan-Adriamycin (CA)-induced inflammation was assessed by measuring circulating levels of IL-1β, TNF-α, IL-6, GCSF, KC, and MCP-1 twenty-four-hours post CA injection. Decline in voluntary wheel running activity (VWRA) from baseline (used as a proxy for fatigue/lethargy), body weight and composition, and food intake were monitored in mice administered four cycles of CA every two weeks with or without DEX. CA increased circulating levels of IL-6, GCSF, KC, and MCP-1 and caused a rapid decline in VWRA and body weight immediately following CA-injection. Although the acute CA-induced decline in VWRA and body weight was not evident in mice administered CA + DEX, DEX alone had a suppressive effect on VWRA, and body weight continued to decline in mice administered both CA and DEX while it returned to baseline in CA-treated mice. CA or DEX alone had no long term impact on VWRA but DEX exacerbated lethargy and weight loss in CA-treated mice. Despite dampening the systemic inflammatory response to chemotherapy, dexamethasone failed to ameliorate acute or long term chemotherapy related fatigue/lethargy. Our pre-clinical findings suggest that supportive therapies like dexamethasone used to acutely control nausea and vomiting in cancer patients may actually contribute to overall symptom burden in cancer patients.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Behavior, Animal; Cyclophosphamide; Dexamethasone; Disease Models, Animal; Doxorubicin; Drug Evaluation, Preclinical; Fatigue; Female; Humans; Lethargy; Mice; Mice, Inbred C57BL; Motor Activity; Nausea; Neoplasms; Vomiting; Weight Loss
PubMed: 29231783
DOI: 10.1080/15384047.2017.1394549