Central Nervous System Depressants
Central Nervous System
Central Nervous System Diseases
Central Nervous System Neoplasms
Nervous System
Brain
Myocardial Depressant Factor
Central Nervous System Infections
Peripheral Nervous System
Neurons
Depression, Chemical
Central Nervous System Viral Diseases
Spinal Cord
Vasculitis, Central Nervous System
Central Nervous System Agents
Pentobarbital
Central Nervous System Fungal Infections
Meprobamate
Enteric Nervous System
Sympathetic Nervous System
Nervous System Physiological Phenomena
Autonomic Nervous System
Nervous System Diseases
Neuroglia
Central Nervous System Bacterial Infections
Barbiturates
Myelin Sheath
Blood-Brain Barrier
Astrocytes
Tuberculosis, Central Nervous System
Nervous System Neoplasms
Hypnotics and Sedatives
Demyelinating Diseases
Rats, Sprague-Dawley
Dose-Response Relationship, Drug
Encephalomyelitis, Autoimmune, Experimental
Molecular Sequence Data
Oligodendroglia
Brain Diseases
Scorpion Venoms
Enflurane
Anesthetics
Immunohistochemistry
Cerebrospinal Fluid
Gene Expression Regulation, Developmental
In Situ Hybridization
Multiple Sclerosis
Cats
Metergoline
Brain Neoplasms
Encephalomyelitis
Cerebral Cortex
Amino Acid Sequence
Microglia
Encephalitis
Encephalitis, Viral
Brain Stem
Synaptic Transmission
Meningoencephalitis
Desipramine
Iontophoresis
Halothane
Seizures
Chlorpromazine
Brain Chemistry
Aminobutyrates
Trauma, Nervous System
Muscle Relaxants, Central
Cells, Cultured
Myelin Proteins
Isoflurane
Respiration
Hippocampus
Disease Models, Animal
Morphine
Peripheral Nerves
Bemegride
RNA, Messenger
Mice, Knockout
Synapses
Norepinephrine
Diazepam
Serotonin
Cerebellum
Rats, Wistar
Meninges
Ciprofloxacin decreases the rate of ethanol elimination in humans. (1/1532)
BACKGROUND: Extrahepatic ethanol metabolism is postulated to take place via microbial oxidation in the colon, mediated by aerobic and facultative anaerobic bacteria. AIMS: To evaluate the role of microbial ethanol oxidation in the total elimination rate of ethanol in humans by reducing gut flora with ciprofloxacin. METHODS: Ethanol was administered intravenously at the beginning and end of a one week period to eight male volunteers. Between ethanol doses volunteers received 750 mg ciprofloxacin twice daily. RESULTS: A highly significant (p=0.001) reduction in the ethanol elimination rate (EER) was detected after ciprofloxacin medication. Mean (SEM) EER was 107.0 (5.3) and 96.9 (4.8) mg/kg/h before and after ciprofloxacin, respectively. Faecal Enterobacteriaceae and Enterococcus sp. were totally absent after medication, and faecal acetaldehyde production capacity was significantly (p<0.05) decreased from 0.91 (0.15) to 0.39 (0.08) nmol/min/mg protein. Mean faecal alcohol dehydrogenase (ADH) activity was significantly (p<0. 05) decreased after medication, but ciprofloxacin did not inhibit human hepatic ADH activity in vitro. CONCLUSIONS: Ciprofloxacin treatment decreased the ethanol elimination rate by 9.4%, with a concomitant decrease in intestinal aerobic and facultative anaerobic bacteria, faecal ADH activity, and acetaldehyde production. As ciprofloxacin has no effect on liver blood flow, hepatic ADH activity, or cytochrome CYP2E1 activity, these effects are probably caused by the reduction in intestinal flora. (+info)Acute effects of ethanol on kainate receptors with different subunit compositions. (2/1532)
Previous studies showed that recombinant homomeric GluR6 receptors are acutely inhibited by ethanol. This study examined the acute actions of ethanol on recombinant homomeric and heteromeric kainate (KA) receptors with different subunit configurations. Application of 25 to 100 mM ethanol produced inhibition of a similar magnitude of both GluR5-Q and GluR6-R KA receptor-dependent currents in Xenopus oocytes. Ethanol decreased the KA Emax without affecting the EC50 and its effect was independent of the membrane holding potential for both of these receptors subtypes. Ethanol also inhibited homomeric and heteromeric receptors transiently expressed in human embryonic kidney (HEK) 293 cells. In these cells, the expression of heteromeric GluR6-R subunit-containing receptors was confirmed by testing their sensitivity to 1 mM alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid. Ethanol inhibited to a similar extent KA-gated currents mediated by receptors composed of either GluR6 or GluR6 + KA1 subunits, and to a slightly lesser extent receptors composed of GluR6 + KA2 subunits. Acute ethanol's effects were tested on GluR5 KA receptors that are expressed as homomers (GluR5-Q) or heteromers (GluR5-R + KA1 and GluR5-R + KA2). Homomeric and heteromeric GluR5 KA receptors were all inhibited to a similar extent by ethanol; however, there was slightly more inhibition of GluR5-R + KA2 receptors. Thus, recombinant KA receptors with different subunit compositions are all acutely inhibited to a similar extent by ethanol. In light of recent reports that KA receptors regulate neurotransmitter release and mediate synaptic currents, we postulate that these receptors may play a role in acute ethanol intoxication. (+info)NMDA receptor characterization and subunit expression in rat cultured mesencephalic neurones. (3/1532)
1. NMDA-induced changes in free intracellular Ca2+ concentration ([Ca2+]i) were determined in individual cultured rat mesencephalic neurones by the fura-2 method. mRNA expression encoding NMDA receptor subunits (NR1, NR2A-D) was examined by RT-PCR. 2. NMDA (1-100 microM, plus 10 microM glycine) induced a concentration-dependent increase in [Ca2+]i (EC50 = 5.7 microM). The effect of NMDA was virtually insensitive to tetrodotoxin (0.3 microM) and nitrendipine (1 microM), but dependent on extracellular Ca2+. 5,7-Dichlorokynurenic acid (10 microM), a specific antagonist at the glycine binding site on the NMDA receptor, abolished the NMDA response. 3. Memantine, an open-channel blocker, and ifenprodil, a preferential non-competitive NR1/NR2B receptor antagonist diminished the NMDA effect with an IC50 value of 0.17 and 1 microM, respectively. Ethanol at 50 and 100 mM caused about 25 and 45%-inhibition, respectively. 4. Agarose gel analysis of the PCR products followed by ethidium bromide fluorescence or CSPD chemiluminescence detection revealed an almost exclusive expression of the NR1 splice variants lacking exon (E) 5 and E22. The 3' splice form without both E21 and E22 exceeded that containing E21 by approximately 4 fold. The relative amounts of NR2A, NR2B, NR2C corresponded to approximately 1:2:1. NR2D mRNA was also detectable. 5. In conclusion, mesencephalic neurones bear ethanol-sensitive NMDA receptors which might be involved in the development of ethanol dependence and withdrawal. The high affinity of NMDA to this receptor, its sensitivity to ifenprodil and memantine may suggest that the mesencephalic NMDA receptor comprises the NR1 splice variant lacking E5, NR2B, and NR2C, respectively. (+info)Effects of alcohol and cholesterol feeding on lipoprotein metabolism and cholesterol absorption in rabbits. (4/1532)
Alcohol fed to rabbits in a liquid formula at 30% of calories increased plasma cholesterol by 36% in the absence of dietary cholesterol and by 40% in the presence of a 0.5% cholesterol diet. The increase was caused almost entirely by VLDL, IDL, and LDL. Cholesterol feeding decreased the fractional catabolic rate for VLDL and LDL apoprotein by 80% and 57%, respectively, and increased the production rate of VLDL and LDL apoprotein by 75% and 15%, respectively. Alcohol feeding had no effect on VLDL apoprotein production but increased LDL production rate by 55%. The efficiency of intestinal cholesterol absorption was increased by alcohol. In the presence of dietary cholesterol, percent cholesterol absorption rose from 34.4+/-2.6% to 44.9+/-2.5% and in the absence of dietary cholesterol, from 84.3+/-1.4% to 88.9+/-1.0%. Increased cholesterol absorption and increased LDL production rate may be important mechanisms for exacerbation by alcohol of hypercholesterolemia in the cholesterol-fed rabbit model. (+info)Mode of action of ICS 205,930, a novel type of potentiator of responses to glycine in rat spinal neurones. (5/1532)
The effect of a novel potentiator of glycine responses, ICS 205,930, was studied by whole-cell recordings from spinal neurones, and compared with that of other known potentiators, in an attempt to differentiate their sites of action. The ability of ICS 205,930 (0.2 microM) to potentiate glycine responses persisted in the presence of concentrations of Zn2+ (5-10 microM) that were saturating for the potentiating effect of this ion. Preincubation with 10 microM Zn2+ before application of glycine plus Zn2+ had an inhibitory effect, which did not result from Zn2+ entry into the neurone, since it persisted with either 10 mM internal EGTA or 10 microM internal Zn2+. To test whether the potentiating effects of ICS 205,930 and Zn2+ interact, both compounds were applied without preincubation. The potentiating effect of ICS 205,930 was similar for responses to glycine and for responses to glycine plus Zn2+, provided the concentrations of agonist were adjusted so as to induce control responses of identical amplitudes. ICS 205,930 remained able to potentiate glycine responses in the presence of ethanol (200 mM). ICS 205,930 also retained its potentiating effect in the presence of the anaesthetic propofol (30 90 microM), which strongly potentiated glycine responses but, in contrast with ICS 205,930, also markedly increased the resting conductance. The anticonvulsant chlormethiazole (50-100 microM) neither potentiated glycine responses nor prevented the effect of ICS 205,930, even though it increased the resting conductance and potentiated GABA(A) responses. The mechanism of action of ICS 205,930 appears to be different from those by which Zn2+, propofol or ethanol potentiate glycine responses. (+info)Sweat ethanol concentrations are highly correlated with co-existing blood values in humans. (6/1532)
This study compared the concentration of ethanol, both absolute and relative to water content, in sweat and blood. Ten male volunteers consumed approximately 13 mmol (kg body weight)-1 of ethanol. Blood and sweat samples were collected approximately 1, 2 and 3 h following ingestion. Sweat was collected following pilocarpine iontophoresis using an anaerobic technique that prevented ethanol evaporation. In addition, the water content of sweat and blood samples was determined. The correlation between sweat and blood ethanol, expressed in mmol l-1, was r = 0.98. The slope of the relationship was 0.81. When corrected for the water content in each sample, and expressed as mmoles per litre of water, the correlation remained very high (r = 0.97) while the slope increased to 1.01. These results suggest that rapid and complete equilibrium of ethanol occurs across the sweat gland epithelium. (+info)Diffusion of dialkylnitrosamines into the rat esophagus as a factor in esophageal carcinogenesis. (7/1532)
To indicate how readily nitrosamines (NAms) diffuse into the esophagus, we measured diffusion rate (flux) through rat esophagus of dialkyl-NAms using side-by-side diffusion apparatuses. Mucosal and serosal flux at 37 degrees C of two NAms, each at 50 microM, was followed for 90 min by gas chromatography-thermal energy analysis of NAms in the receiver chamber. Mucosal flux of one or two NAms at a time gave identical results. Mucosal flux was highest for the strong esophageal carcinogens methyl-n-amyl-NAm (MNAN) and methylbenzyl-NAm. Mucosal esophageal flux of 11 NAms was 18-280 times faster and flux of two NAms through skin was 13-28 times faster than that predicted for skin from the molecular weights and octanol:water partition coefficients, which were also measured. Mucosal: serosal flux ratio was correlated (P < 0.05) with esophageal carcinogenicity and molecular weight. For seven NAms tested for carcinogenicity by Druckrey et al. [(1967) Z. Krebsforsch., 69, 103-201], mucosal flux was correlated with esophageal carcinogenicity with borderline significance (P = 0.07). The MNAN:dipropyl-NAm ratio for mucosal esophageal flux was unaffected when rats were treated with phenethylisothiocyanate and was similar to that for forestomach, indicating no involvement by cytochromes P450. Mucosal esophageal flux of MNAN and dimethyl-NAm was reduced by >90% on enzymic removal of the stratum corneum, was unaffected by 0.1 mM verapamil and was inhibited 67-94% by 1.0 mM KCN and 82-93% by 0.23% ethanol. NAm flux through rat skin and jejunum was 5-17% of that through esophagus. Flux through skin increased 5-13 times after enzymic or mechanical removal of the epidermis; the histology probably explained this difference from esophagus. Hence, NAms could be quite rapidly absorbed by human esophagus when NAm-containing foods or beverages are swallowed, the esophageal carcinogenicity of NAms may be partly determined by their esophageal flux and NAm flux probably occurs by passive diffusion. (+info)Dental anesthetic management of a patient with ventricular arrhythmias. (8/1532)
During routine deep sedation for endodontic therapy, a dentist-anesthesiologist observed premature ventricular contractions (PVCs) on a 62-yr-old woman's electrocardiogram (EKG) tracing. The dentist was able to complete the root canal procedure under intravenous (i.v.) sedation without any problems. The dentist-anesthesiologist referred the patient for medical evaluation. She was found to be free from ischemic cardiac disease with normal ventricular function. The patient was cleared to continue her dental treatment with deep sedation. She subsequently continued to undergo dental treatment with deep intravenous sedation without incident, although her EKG exhibited frequent PVCs, up to 20 per minute, including couplets and episodes of trigeminy. This article will review indications for medical intervention, antiarrhythmic medications, and anesthetic interventions for perioperative PVCs. (+info)1. Neurodegenerative diseases: These are diseases that cause progressive loss of brain cells, leading to cognitive decline and motor dysfunction. Examples include Alzheimer's disease, Parkinson's disease, and Huntington's disease.
2. Stroke: A stroke occurs when blood flow to the brain is interrupted, leading to cell death and potential long-term disability.
3. Traumatic brain injury: This type of injury occurs when the brain is subjected to a sudden and forceful impact, such as in a car accident or fall.
4. Infections: Bacterial, viral, and fungal infections can all cause CNS diseases, such as meningitis and encephalitis.
5. Autoimmune disorders: These are conditions in which the immune system mistakenly attacks healthy cells in the brain, leading to inflammation and damage. Examples include multiple sclerosis and lupus.
6. Brain tumors: Tumors can occur in any part of the brain and can be benign or malignant.
7. Cerebrovascular diseases: These are conditions that affect the blood vessels in the brain, such as aneurysms and arteriovenous malformations (AVMs).
8. Neurodevelopmental disorders: These are conditions that affect the development of the brain and nervous system, such as autism spectrum disorder and attention deficit hyperactivity disorder (ADHD).
CNS diseases can have a significant impact on quality of life, and some can be fatal. Treatment options vary depending on the specific diagnosis and severity of the disease. Some CNS diseases can be managed with medication, while others may require surgery or other interventions.
Benign CNS neoplasms include:
1. Meningiomas: These are the most common type of benign CNS tumor, arising from the meninges (the membranes covering the brain and spinal cord).
2. Acoustic neuromas: These tumors arise from the nerve cells that connect the inner ear to the brain.
3. Pineal gland tumors: These are rare tumors that occur in the pineal gland, a small gland located in the brain.
4. Craniopharyngiomas: These are rare tumors that arise from the remnants of the embryonic pituitary gland and can cause a variety of symptoms including headaches, vision loss, and hormonal imbalances.
Malignant CNS neoplasms include:
1. Gliomas: These are the most common type of malignant CNS tumor and arise from the supporting cells of the brain called glial cells. Examples of gliomas include astrocytomas, oligodendrogliomas, and medulloblastomas.
2. Lymphomas: These are cancers of the immune system that can occur in the CNS.
3. Melanomas: These are rare tumors that arise from the pigment-producing cells of the skin and can spread to other parts of the body, including the CNS.
4. Metastatic tumors: These are tumors that have spread to the CNS from other parts of the body, such as the breast, lung, or colon.
The diagnosis and treatment of central nervous system neoplasms depend on the type, size, location, and severity of the tumor, as well as the patient's overall health and medical history. Treatment options can include surgery, radiation therapy, chemotherapy, targeted therapy, and immunotherapy.
The prognosis for CNS neoplasms varies depending on the type of tumor and the effectiveness of treatment. In general, gliomas have a poorer prognosis than other types of CNS tumors, with five-year survival rates ranging from 30% to 60%. Lymphomas and melanomas have better prognoses, with five-year survival rates of up to 80%. Metastatic tumors have a more guarded prognosis, with five-year survival rates depending on the primary site of the cancer.
In summary, central nervous system neoplasms are abnormal growths of tissue in the brain and spinal cord that can cause a variety of symptoms and can be benign or malignant. The diagnosis and treatment of these tumors depend on the type, size, location, and severity of the tumor, as well as the patient's overall health and medical history. The prognosis for CNS neoplasms varies depending on the type of tumor and the effectiveness of treatment, but in general, gliomas have a poorer prognosis than other types of CNS tumors.
The most common types of CNS infections include:
1. Meningitis: Inflammation of the protective membranes (meninges) that cover the brain and spinal cord, often caused by bacteria or viruses.
2. Encephalitis: Inflammation of the brain tissue itself, usually caused by a virus.
3. Abscesses: Pockets of pus that form in the brain or spinal cord, typically caused by bacterial infections.
4. Cryptococcal infections: Caused by a fungus called Cryptococcus neoformans, often affecting people with weakened immune systems.
5. Toxoplasmosis: A parasitic infection caused by the Toxoplasma gondii parasite, which can affect the CNS in people with compromised immune systems.
Symptoms of CNS infections can vary depending on the specific type and severity of the infection, but may include fever, headache, confusion, seizures, weakness, and stiff neck. Diagnosis is typically made through a combination of physical examination, laboratory tests, and imaging studies such as CT or MRI scans.
Treatment of CNS infections depends on the underlying cause, but may involve antibiotics, antiviral medications, or antifungal drugs. In severe cases, hospitalization and supportive care such as intravenous fluids, oxygen therapy, and respiratory support may be necessary.
Prevention of CNS infections includes good hygiene practices such as frequent handwashing, avoiding close contact with people who are sick, and getting vaccinated against certain viruses that can cause CNS infections. Early diagnosis and prompt treatment are critical to preventing long-term complications of CNS infections and improving outcomes for patients.
Some common examples of CNSVD include:
1. Herpes simplex virus (HSV) encephalitis: This is an inflammation of the brain caused by the herpes simplex virus. It can cause fever, headache, confusion, and seizures.
2. West Nile virus (WNV) encephalitis: This is an infection of the brain caused by the West Nile virus, which is transmitted through the bite of an infected mosquito. Symptoms can include fever, headache, muscle weakness, and confusion.
3. Japanese encephalitis (JE): This is a viral infection that affects the brain and is transmitted through the bite of an infected mosquito. Symptoms can include fever, headache, seizures, and changes in behavior or cognitive function.
4. Rabies: This is a viral infection that affects the brain and is transmitted through the bite of an infected animal, usually a dog, bat, or raccoon. Symptoms can include fever, headache, agitation, and changes in behavior or cognitive function.
5. Enteroviral encephalitis: This is an infection of the brain caused by enteroviruses, which are common viruses that affect the gastrointestinal tract. Symptoms can include fever, vomiting, diarrhea, and changes in behavior or cognitive function.
The diagnosis of CNSVD typically involves a combination of physical examination, laboratory tests (such as blood tests or lumbar puncture), and imaging studies (such as CT or MRI scans). Treatment options vary depending on the specific disease and may include antiviral medications, supportive care, and rehabilitation.
Prevention of CNSVD includes avoiding exposure to mosquitoes and other vectors that can transmit disease, maintaining good hygiene practices (such as washing hands frequently), and getting vaccinated against diseases such as rabies and measles. In addition, taking steps to prevent head trauma and using protective equipment when engaging in activities that involve risk of head injury can help reduce the risk of CNSVD.
Overall, while central nervous system viral diseases can be serious and potentially life-threatening, early diagnosis and treatment can improve outcomes and prevent long-term complications. It is important to seek medical attention promptly if symptoms persist or worsen over time.
The exact cause of CNS vasculitis is not fully understood, but it is believed to be an autoimmune disorder, meaning that the immune system mistakenly attacks healthy tissues in the CNS. The condition can occur at any age, but it most commonly affects adults between the ages of 40 and 60.
Symptoms of CNS vasculitis can vary depending on the location and severity of the inflammation, but may include:
* Headaches
* Confusion
* Memory loss
* Seizures
* Weakness or numbness in the limbs
* Vision problems
* Speech difficulties
Diagnosis of CNS vasculitis typically involves a combination of physical examination, medical history, and diagnostic tests such as MRI or CT scans, lumbar puncture, and blood tests. Treatment options for CNS vasculitis vary depending on the severity of the condition and may include corticosteroids, immunosuppressive drugs, and plasmapheresis. In severe cases, surgery may be necessary to relieve pressure on the brain or spinal cord.
Overall, CNS vasculitis is a serious condition that can have significant neurological consequences if left untreated. Early diagnosis and aggressive treatment are critical to prevent long-term damage and improve outcomes for patients with this condition.
The most common types of CNS fungal infections include:
1. Meningitis: An inflammation of the membranes that cover the brain and spinal cord, caused by fungi such as Candida, Aspergillus, or Cryptococcus.
2. Encephalitis: An inflammation of the brain tissue itself, caused by fungi such as Histoplasma or Coccidioides.
3. Abscesses: Pocket of pus that form in the brain or spinal cord, caused by bacteria or fungi.
4. Opportunistic infections: Infections that occur in people with compromised immune systems, such as HIV/AIDS patients or those taking immunosuppressive drugs after an organ transplant.
CNS fungal infections can cause a wide range of symptoms, including headache, fever, confusion, seizures, and loss of coordination. They are typically diagnosed through a combination of physical examination, laboratory tests, and imaging studies such as CT or MRI scans.
Treatment of CNS fungal infections usually involves the use of antifungal medications, which can be administered intravenously or orally. The choice of treatment depends on the severity and location of the infection, as well as the patient's overall health status. In some cases, surgery may be necessary to drain abscesses or relieve pressure on the brain.
Prevention of CNS fungal infections is important for individuals at risk, such as those with compromised immune systems or underlying medical conditions. This includes taking antifungal medications prophylactically, avoiding exposure to fungal spores, and practicing good hygiene.
Overall, CNS fungal infections are serious and potentially life-threatening conditions that require prompt diagnosis and treatment. With appropriate management, many patients can recover fully, but delays in diagnosis and treatment can lead to poor outcomes.
Examples of Nervous System Diseases include:
1. Alzheimer's disease: A progressive neurological disorder that affects memory and cognitive function.
2. Parkinson's disease: A degenerative disorder that affects movement, balance and coordination.
3. Multiple sclerosis: An autoimmune disease that affects the protective covering of nerve fibers.
4. Stroke: A condition where blood flow to the brain is interrupted, leading to brain cell death.
5. Brain tumors: Abnormal growth of tissue in the brain.
6. Neuropathy: Damage to peripheral nerves that can cause pain, numbness and weakness in hands and feet.
7. Epilepsy: A disorder characterized by recurrent seizures.
8. Motor neuron disease: Diseases that affect the nerve cells responsible for controlling voluntary muscle movement.
9. Chronic pain syndrome: Persistent pain that lasts more than 3 months.
10. Neurodevelopmental disorders: Conditions such as autism, ADHD and learning disabilities that affect the development of the brain and nervous system.
These diseases can be caused by a variety of factors such as genetics, infections, injuries, toxins and ageing. Treatment options for Nervous System Diseases range from medications, surgery, rehabilitation therapy to lifestyle changes.
CNS bacterial infections can cause a wide range of symptoms, including fever, headache, confusion, seizures, and loss of consciousness. In severe cases, these infections can lead to meningitis, encephalitis, or abscesses in the brain or spinal cord.
The diagnosis of CNS bacterial infections is based on a combination of clinical findings, laboratory tests, and imaging studies. Laboratory tests may include blood cultures, cerebrospinal fluid (CSF) cultures, and polymerase chain reaction (PCR) tests to identify the causative bacteria. Imaging studies, such as computed tomography (CT) or magnetic resonance imaging (MRI), may be used to visualize the extent of the infection.
Treatment of CNS bacterial infections typically involves the use of antibiotics, which can help to clear the infection and prevent further complications. In some cases, surgical intervention may be necessary to drain abscesses or relieve pressure on the brain or spinal cord.
Preventive measures for CNS bacterial infections include vaccination against certain types of bacteria, such as Streptococcus pneumoniae and Haemophilus influenzae, good hygiene practices, and appropriate use of antibiotics. Early diagnosis and treatment are critical to preventing long-term neurological damage or death.
In conclusion, CNS bacterial infections can be serious and potentially life-threatening conditions that require prompt diagnosis and treatment. Understanding the causes, symptoms, diagnosis, treatment, and prevention of these infections is essential for effective management and optimal outcomes for patients affected by them.
The symptoms of TB CNS can vary depending on the location and severity of the infection, but may include:
* Headache
* Fever
* Nausea and vomiting
* Weakness or paralysis of the face, arm, or leg
* Confusion, seizures, or coma
* Vision loss or double vision
* Hearing loss or ringing in the ears
* Meningitis (inflammation of the protective membranes covering the brain and spinal cord)
TB CNS can be difficult to diagnose because the symptoms are often non-specific and can resemble other conditions, such as a stroke or a brain tumor. A diagnosis is typically made through a combination of physical examination, imaging tests (such as CT or MRI scans), and laboratory tests (such as lumbar puncture and culture).
TB CNS is treated with antibiotics, usually for a period of at least 6-12 months. In some cases, surgery may be necessary to remove abscesses or repair damaged tissue. Treatment outcomes are generally good if the diagnosis is made early and the infection is contained within the central nervous system. However, delays in diagnosis and treatment can lead to serious complications, such as permanent neurological damage or death.
Prevention of TB CNS involves identifying and treating cases of active TB infection, as well as taking measures to prevent the spread of the disease. This includes screening for TB in high-risk individuals, such as those with weakened immune systems or living in areas with a high prevalence of TB. Vaccination against TB is also recommended in some cases.
In summary, TB CNS is a rare and potentially life-threatening form of tuberculosis that can cause severe neurological symptoms and complications. Early diagnosis and treatment are critical to preventing serious outcomes and ensuring effective management of the disease.
Some common types of nervous system neoplasms include:
1. Brain tumors: These are abnormal growths that develop in the brain, including gliomas (such as glioblastoma), meningiomas, and acoustic neuromas.
2. Spinal cord tumors: These are abnormal growths that develop in the spinal cord, including astrocytomas, oligodendrogliomas, and metastatic tumors.
3. Nerve sheath tumors: These are abnormal growths that develop in the covering of nerves, such as neurofibromas and schwannomas.
4. Pineal gland tumors: These are abnormal growths that develop in the pineal gland, a small endocrine gland located in the brain.
Symptoms of nervous system neoplasms can vary depending on their location and size, but may include headaches, seizures, weakness or numbness in the arms or legs, and changes in vision, speech, or balance. Diagnosis is typically made through a combination of imaging studies (such as MRI or CT scans) and tissue biopsy. Treatment options vary depending on the type and location of the tumor, but may include surgery, radiation therapy, and chemotherapy.
In summary, nervous system neoplasms are abnormal growths that can develop in the brain, spinal cord, and nerves, and can have a significant impact on the body. Diagnosis and treatment require a comprehensive approach, involving a team of medical professionals with expertise in neurology, neurosurgery, radiation oncology, and other related specialties.
The most common demyelinating diseases include:
1. Multiple sclerosis (MS): An autoimmune disease that affects the CNS, including the brain, spinal cord, and optic nerves. MS causes inflammation and damage to the myelin sheath, leading to a range of symptoms such as muscle weakness, vision problems, and cognitive difficulties.
2. Acute demyelination: A sudden, severe loss of myelin that can be caused by infections, autoimmune disorders, or other factors. This condition can result in temporary or permanent nerve damage.
3. Chronic inflammatory demyelination (CIDP): A rare autoimmune disorder that causes progressive damage to the myelin sheath over time. CIDP can affect the CNS and the peripheral nervous system (PNS).
4. Moore's disease: A rare genetic disorder that results in progressive demyelination of the CNS, leading to a range of neurological symptoms including muscle weakness, seizures, and cognitive difficulties.
5. Leukodystrophies: A group of genetic disorders that affect the development or function of myelin-producing cells in the CNS. These conditions can cause progressive loss of myelin and result in a range of neurological symptoms.
Demyelinating diseases can be challenging to diagnose, as the symptoms can be similar to other conditions and the disease progression can be unpredictable. Treatment options vary depending on the specific condition and its severity, and may include medications to reduce inflammation and modulate the immune system, as well as rehabilitation therapies to help manage symptoms and improve quality of life.
The disease is typically induced in laboratory animals such as mice or rats by immunizing them with myelin proteins, such as myelin basic protein (MBP) or proteolipid protein (PLP), emulsified in adjuvants. The resulting immune response leads to the production of autoantibodies and activated T cells that cross the blood-brain barrier and attack the CNS.
EAE is used as a model for MS because it shares many similarities with the human disease, including:
1. Demyelination: EAE induces demyelination of nerve fibers in the CNS, which is also a hallmark of MS.
2. Autoimmune response: The immune response in EAE is triggered by autoantigens, similar to MS.
3. Chronic course: EAE is a chronic disease with recurrent relapses, similar to MS.
4. Lesion distribution: EAE lesions are distributed throughout the CNS, including the cerebral cortex, cerebellum, brainstem, and spinal cord, which is also true for MS.
EAE has been used extensively in the study of MS to investigate the immunopathogenesis of the disease, to develop new diagnostic markers and treatments, and to test the efficacy of potential therapeutic agents.
Some common types of brain diseases include:
1. Neurodegenerative diseases: These are progressive conditions that damage or kill brain cells over time, leading to memory loss, cognitive decline, and movement disorders. Examples include Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis (ALS).
2. Stroke: This occurs when blood flow to the brain is interrupted, leading to cell death and potential long-term disability.
3. Traumatic brain injury (TBI): This refers to any type of head injury that causes damage to the brain, such as concussions, contusions, or penetrating wounds.
4. Infections: Viral, bacterial, and fungal infections can all affect the brain, leading to a range of symptoms including fever, seizures, and meningitis.
5. Tumors: Brain tumors can be benign or malignant and can cause a variety of symptoms depending on their location and size.
6. Cerebrovascular diseases: These conditions affect the blood vessels of the brain, leading to conditions such as aneurysms, arteriovenous malformations (AVMs), and Moyamoya disease.
7. Neurodevelopmental disorders: These are conditions that affect the development of the brain and nervous system, such as autism spectrum disorder, ADHD, and intellectual disability.
8. Sleep disorders: Conditions such as insomnia, narcolepsy, and sleep apnea can all have a significant impact on brain function.
9. Psychiatric disorders: Mental health conditions such as depression, anxiety, and schizophrenia can affect the brain and its functioning.
10. Neurodegenerative with brain iron accumulation: Conditions such as Parkinson's disease, Alzheimer's disease, and Huntington's disease are characterized by the accumulation of abnormal proteins and other substances in the brain, leading to progressive loss of brain function over time.
It is important to note that this is not an exhaustive list and there may be other conditions or factors that can affect the brain and its functioning. Additionally, many of these conditions can have a significant impact on a person's quality of life, and it is important to seek medical attention if symptoms persist or worsen over time.
The symptoms of MS can vary widely depending on the location and severity of the damage to the CNS. Common symptoms include:
* Weakness, numbness, or tingling in the limbs
* Fatigue
* Vision problems, such as blurred vision, double vision, or loss of vision
* Difficulty with balance and coordination
* Tremors or spasticity
* Memory and concentration problems
* Mood changes, such as depression or mood swings
* Bladder and bowel problems
There is no cure for MS, but various treatments can help manage the symptoms and slow the progression of the disease. These treatments include:
* Disease-modifying therapies (DMTs) - These medications are designed to reduce the frequency and severity of relapses, and they can also slow the progression of disability. Examples of DMTs include interferons, glatiramer acetate, natalizumab, fingolimod, dimethyl fumarate, teriflunomide, and alemtuzumab.
* Steroids - Corticosteroids can help reduce inflammation during relapses, but they are not a long-term solution.
* Pain management medications - Pain relievers, such as acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs), can help manage pain caused by MS.
* Muscle relaxants - These medications can help reduce spasticity and tremors.
* Physical therapy - Physical therapy can help improve mobility, balance, and strength.
* Occupational therapy - Occupational therapy can help with daily activities and assistive devices.
* Speech therapy - Speech therapy can help improve communication and swallowing difficulties.
* Psychological counseling - Counseling can help manage the emotional and psychological aspects of MS.
It's important to note that each person with MS is unique, and the best treatment plan will depend on the individual's specific symptoms, needs, and preferences. It's essential to work closely with a healthcare provider to find the most effective treatment plan.
Brain neoplasms can arise from various types of cells in the brain, including glial cells (such as astrocytes and oligodendrocytes), neurons, and vascular tissues. The symptoms of brain neoplasms vary depending on their size, location, and type, but may include headaches, seizures, weakness or numbness in the limbs, and changes in personality or cognitive function.
There are several different types of brain neoplasms, including:
1. Meningiomas: These are benign tumors that arise from the meninges, the thin layers of tissue that cover the brain and spinal cord.
2. Gliomas: These are malignant tumors that arise from glial cells in the brain. The most common type of glioma is a glioblastoma, which is aggressive and hard to treat.
3. Pineal parenchymal tumors: These are rare tumors that arise in the pineal gland, a small endocrine gland in the brain.
4. Craniopharyngiomas: These are benign tumors that arise from the epithelial cells of the pituitary gland and the hypothalamus.
5. Medulloblastomas: These are malignant tumors that arise in the cerebellum, specifically in the medulla oblongata. They are most common in children.
6. Acoustic neurinomas: These are benign tumors that arise on the nerve that connects the inner ear to the brain.
7. Oligodendrogliomas: These are malignant tumors that arise from oligodendrocytes, the cells that produce the fatty substance called myelin that insulates nerve fibers.
8. Lymphomas: These are cancers of the immune system that can arise in the brain and spinal cord. The most common type of lymphoma in the CNS is primary central nervous system (CNS) lymphoma, which is usually a type of B-cell non-Hodgkin lymphoma.
9. Metastatic tumors: These are tumors that have spread to the brain from another part of the body. The most common types of metastatic tumors in the CNS are breast cancer, lung cancer, and melanoma.
These are just a few examples of the many types of brain and spinal cord tumors that can occur. Each type of tumor has its own unique characteristics, such as its location, size, growth rate, and biological behavior. These factors can help doctors determine the best course of treatment for each patient.
The symptoms of encephalomyelitis can vary depending on the cause and severity of the condition. Common symptoms include fever, headache, neck stiffness, muscle weakness, confusion, seizures, and loss of sensation or paralysis in parts of the body. In severe cases, encephalomyelitis can lead to life-threatening complications such as brain damage, stroke, and respiratory failure.
The diagnosis of encephalomyelitis is based on a combination of clinical features, laboratory tests, and imaging studies. Laboratory tests may include blood tests to detect the presence of inflammatory markers or antibodies against specific infectious agents. Imaging studies such as CT or MRI scans can help to identify inflammation in the brain and spinal cord.
Treatment of encephalomyelitis depends on the underlying cause of the condition. In some cases, antiviral medications may be used to treat infections such as herpes simplex or West Nile virus. In other cases, corticosteroids may be prescribed to reduce inflammation and prevent further damage. Supportive care such as intravenous fluids, oxygen therapy, and physical therapy may also be necessary to manage symptoms and promote recovery.
In conclusion, encephalomyelitis is a serious condition that can cause significant morbidity and mortality. Early diagnosis and prompt treatment are essential to prevent complications and improve outcomes for patients with this condition.
Encephalitis can cause a range of symptoms, including fever, headache, confusion, seizures, and loss of consciousness. In severe cases, encephalitis can lead to brain damage, coma, and even death.
The diagnosis of encephalitis is based on a combination of clinical signs, laboratory tests, and imaging studies. Laboratory tests may include blood tests to detect the presence of antibodies or antigens specific to the causative agent, as well as cerebrospinal fluid (CSF) analysis to look for inflammatory markers and/or bacteria or viruses in the CSF. Imaging studies, such as CT or MRI scans, may be used to visualize the brain and identify any areas of damage or inflammation.
Treatment of encephalitis typically involves supportive care, such as intravenous fluids, oxygen therapy, and medication to manage fever and pain. Antiviral or antibacterial drugs may be used to target the specific causative agent, if identified. In severe cases, hospitalization in an intensive care unit (ICU) may be necessary to monitor and manage the patient's condition.
Prevention of encephalitis includes vaccination against certain viruses that can cause the condition, such as herpes simplex virus and Japanese encephalitis virus. Additionally, avoiding exposure to mosquitoes and other insects that can transmit viruses or bacteria that cause encephalitis, as well as practicing good hygiene and sanitation, can help reduce the risk of infection.
Overall, encephalitis is a serious and potentially life-threatening condition that requires prompt medical attention for proper diagnosis and treatment. With appropriate care, many patients with encephalitis can recover fully or partially, but some may experience long-term neurological complications or disability.
A type of encephalitis caused by a virus that inflames the brain and spinal cord, leading to fever, headache, confusion, seizures, and in severe cases, coma or death. Viral encephalitis is usually transmitted through the bite of an infected mosquito or tick, but can also be spread through contact with infected blood or organs. Diagnosis is made through a combination of physical examination, laboratory tests, and imaging studies. Treatment typically involves supportive care, such as intravenous fluids, oxygen therapy, and medication to manage fever and seizures, as well as antiviral medications in severe cases.
Synonyms: viral encephalitis
Antonyms: bacterial encephalitis
Similar term: meningitis
The symptoms of meningoencephalitis can vary depending on the cause, but common signs include fever, headache, stiff neck, confusion, seizures, and loss of consciousness. The disease can progress rapidly and can be fatal if not treated promptly.
Diagnosis is typically made through a combination of physical examination, laboratory tests (such as blood cultures and PCR), and imaging studies (such as CT or MRI scans). Treatment options depend on the underlying cause, but may include antibiotics, antiviral medications, and supportive care to manage symptoms and prevent complications.
Prognosis for meningoencephalitis depends on the severity of the disease and the promptness and effectiveness of treatment. In general, the prognosis is better for patients who receive prompt medical attention and have a mild form of the disease. However, the disease can be severe and potentially life-threatening, especially in young children, older adults, and those with weakened immune systems.
There are many different types of seizures, each with its own unique set of symptoms. Some common types of seizures include:
1. Generalized seizures: These seizures affect both sides of the brain and can cause a range of symptoms, including convulsions, loss of consciousness, and muscle stiffness.
2. Focal seizures: These seizures affect only one part of the brain and can cause more specific symptoms, such as weakness or numbness in a limb, or changes in sensation or vision.
3. Tonic-clonic seizures: These seizures are also known as grand mal seizures and can cause convulsions, loss of consciousness, and muscle stiffness.
4. Absence seizures: These seizures are also known as petit mal seizures and can cause a brief loss of consciousness or staring spell.
5. Myoclonic seizures: These seizures can cause sudden, brief muscle jerks or twitches.
6. Atonic seizures: These seizures can cause a sudden loss of muscle tone, which can lead to falls or drops.
7. Lennox-Gastaut syndrome: This is a rare and severe form of epilepsy that can cause multiple types of seizures, including tonic, atonic, and myoclonic seizures.
Seizures can be diagnosed through a combination of medical history, physical examination, and diagnostic tests such as electroencephalography (EEG) or imaging studies. Treatment for seizures usually involves anticonvulsant medications, but in some cases, surgery or other interventions may be necessary.
Overall, seizures are a complex and multifaceted symptom that can have a significant impact on an individual's quality of life. It is important to seek medical attention if you or someone you know is experiencing seizures, as early diagnosis and treatment can help to improve outcomes and reduce the risk of complications.
Trauma to the nervous system can have a profound impact on an individual's quality of life, and can lead to a range of symptoms including:
* Headaches
* Dizziness and vertigo
* Memory loss and difficulty concentrating
* Mood changes such as anxiety, depression, or irritability
* Sleep disturbances
* Changes in sensation, such as numbness or tingling
* Weakness or paralysis of certain muscle groups
Trauma to the nervous system can also have long-lasting effects, and may lead to chronic conditions such as post-traumatic stress disorder (PTSD), chronic pain, and fibromyalgia.
Treatment for trauma to the nervous system will depend on the specific nature of the injury and the severity of the symptoms. Some common treatments include:
* Medication to manage symptoms such as pain, anxiety, or depression
* Physical therapy to help regain strength and mobility
* Occupational therapy to help with daily activities and improve function
* Cognitive-behavioral therapy (CBT) to address any emotional or psychological issues
* Alternative therapies such as acupuncture, massage, or meditation to help manage symptoms and promote relaxation.
It's important to seek medical attention if you experience any symptoms of trauma to the nervous system, as prompt treatment can help reduce the risk of long-term complications and improve outcomes.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
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Benzodiazepines4
- In this cohort of HIV-infected and at-risk HIV-uninfected women, use of benzodiazepines, CNS depressants, and conditional QTc interval-prolonging medications were associated with a higher risk of mortality independent of methadone and other well-recognized mortality risk factors. (nih.gov)
- When benzodiazepines are consumed with alcohol, overdose can result from the impact of two central nervous system depressants. (narconon.org)
- Benzodiazepines are a depressant. (narconon.org)
- Benzodiazepines like Xanax are central nervous system depressants that slow down brain activity by increasing gamma-aminobutyric acid (GABA). (mountainside.com)
Prescription CNS depressants5
- What are prescription CNS depressants? (nih.gov)
- How do people use and misuse prescription CNS depressants? (nih.gov)
- Most prescription CNS depressants come in pill, capsule, or liquid form, which a person takes by mouth. (nih.gov)
- Yes, use or misuse of prescription CNS depressants can lead to problem use, known as a substance use disorder (SUD) , which takes the form of addiction in severe cases. (nih.gov)
- Long-term use of prescription CNS depressants, even as prescribed by a doctor, can cause some people to develop a tolerance, which means that they need higher and/or more frequent doses of the drug to get the desired effects. (nih.gov)
Alcohol8
- Cancer risk: Drug and alcohol use increases the chance of developing various cancers that can damage sexual function and the reproductive system. (passagesmalibu.com)
- Alcohol is a central nervous system depressant that changes the way you think and act. (nih.gov)
- Delirium tremens is a severe form of alcohol withdrawal that involves sudden and severe mental or nervous system changes. (wikidoc.org)
- Karbinal ER may interact with monoamine oxidase inhibitors (MAOIs), alcohol, hypnotics, sedatives, tranquilizers or other substances that suppress the central nervous system . (rxlist.com)
- Alcohol is a depressant. (narconon.org)
- Although this interaction is still being examined, one study reveals that ethanol, the main ingredient in alcohol, may increase the concentration of alprazolam in your system. (mountainside.com)
- Many of the herbalists who sell Amphetamine will arrange for medical testing or treatment The two most commonly used depressants are alcohol and tobacco. (bigkahunaadventures.com)
- Alcohol, the shortened term for ethyl alcohol, is a depressant that slows the activity of the central nervous system and the brain. (ursinus.edu)
Sedatives1
- Central Nervous System (CNS) depressants are medicines that include sedatives, tranquilizers, and hypnotics. (nih.gov)
Slows1
- When people overdose on a CNS depressant, their breathing often slows or stops. (nih.gov)
Overdose2
Drugs2
- A very loosely defined group of drugs that tend to reduce the activity of the central nervous system. (nih.gov)
- The layperson might not realize it, but consuming two depressant drugs at once can have severe, even lethal consequences. (narconon.org)
Severe1
- and severe or fatal pulmonary, gastrointestinal, central nervous system and vaginal bleeding (hemorrhage). (pdr.net)
Addiction1
- Can prescription CNS depressant use lead to addiction and substance use disorder? (nih.gov)
Gamma-amin1
- Most CNS depressants act on the brain by increasing activity of gamma-aminobutyric acid (GABA), a chemical that inhibits brain activity. (nih.gov)
Medications1
- To evaluate the association between use of methadone, other central nervous system (CNS) depressants, and QTc interval-prolonging medications and risk of mortality among human immunodeficiency virus (HIV)-infected and at-risk HIV-uninfected women. (nih.gov)
Substance1
- Other infectious illnesses can affect the reproductive system due to hazardous behaviors or a lack of personal cleanliness or personal care due to a substance use issue. (passagesmalibu.com)
Clinical1
- The FDA cleared the first seven tesla (7T) magnetic resonance imaging (MRI) device, more than doubling the static magnetic field strength available for use in the U.S. The Magnetom Terra is the first 7T MRI system cleared for clinical use in the U.S. The Magnetom Terra is for patients who weigh more than 66 pounds and is limited to examinations of the head, arms and legs (extremities). (pdr.net)
Effects5
- People who start taking CNS depressants usually feel sleepy and uncoordinated for the first few days until the body adjusts to these side effects. (nih.gov)
- If a person takes CNS depressants long term, he or she might need larger doses to achieve therapeutic effects. (nih.gov)
- Hypoxia can have short- and long-term mental effects and effects on the nervous system, including coma and permanent brain damage. (nih.gov)
- Enhanced CNS depressant effects. (medscape.com)
- For the purposes of this PA, psychoactive natural products are defined as fungus- or plant-derived products that are taken primarily for their effects on the central nervous system (e.g., stimulant, depressant, and/or hallucinogenic effects), rather than for treatment, medicinal or therapeutic effects. (nih.gov)
Brain5
- How do CNS depressants affect the brain? (nih.gov)
- Many of the characteristics of pain have been associated with specific brain systems, although much remains to be learned. (nih.gov)
- Additionally, researchers have found that many of the brain systems involved with the experience of pain overlap with the experience of basic emotions. (nih.gov)
- Consequently, when people experience undesirable emotions (e.g., fear, anxiety, anger), the same brain systems responsible for these emotions also amplify the experience of pain. (nih.gov)
- Fortunately, there also are systems in the brain that help to dampen or decrease pain. (nih.gov)
Patients1
- The system is intended to be used in conjunction with outpatient therapy and in addition to a contingency management system, a widely-used program for treating SUDs that uses a series of incentives to reward patients for adherence to their treatment program. (pdr.net)
Effect2
Patient1
- The Reset device is a mobile medical application system containing a patient application and clinician dashboard. (pdr.net)
Results1
- An eye disease that results in a loss of central, "straight-ahead" vision. (nih.gov)
Experience1
- Those who have become addicted to a prescription CNS depressant and stop using the drug abruptly may experience a withdrawal. (nih.gov)
Xanax1
- Xanax is a benzodiazepine the central nervous system.It is generally prescribed to indivi. (drugnet.net)
Time1
- You may submit questions through the Webinar system at any time during the presentation by selecting the Q and A tab at the top of the Webinar screen and typing in your question. (cdc.gov)
Disorder2
Doses2
- If a person takes CNS depressants long term, he or she might need larger doses to achieve therapeutic effects. (nih.gov)
- Long-term use of prescription CNS depressants, even as prescribed by a doctor, can cause some people to develop a tolerance, which means that they need higher and/or more frequent doses of the drug to get the desired effects. (nih.gov)
Activity2
- Most CNS depressants act on the brain by increasing activity of gamma-aminobutyric acid (GABA), a chemical that inhibits brain activity. (nih.gov)
- During normal awake respiration, the obstructive tendency of the negative inspiratory pressure within the upper airway is balanced by the outward force of pharyngeal dilator muscle activity under central nervous system (CNS) control. (medscape.com)
Patients1
- Gabapentin has been effective in patients with central nervous system (CNS) lesions and in some other groups. (medscape.com)
Muscle1
- Ketamine acts on the cortex and limbic system, decreasing muscle spasms. (medscape.com)