A GAMMA-AMINOBUTYRIC ACID derivative that is a specific agonist of GABA-B RECEPTORS. It is used in the treatment of MUSCLE SPASTICITY, especially that due to SPINAL CORD INJURIES. Its therapeutic effects result from actions at spinal and supraspinal sites, generally the reduction of excitatory transmission.
Endogenous compounds and drugs that bind to and activate GABA-B RECEPTORS.
Endogenous compounds and drugs that bind to and activate GAMMA-AMINOBUTYRIC ACID receptors (RECEPTORS, GABA).
A heterogeneous group of drugs used to produce muscle relaxation, excepting the neuromuscular blocking agents. They have their primary clinical and therapeutic uses in the treatment of muscle spasm and immobility associated with strains, sprains, and injuries of the back and, to a lesser degree, injuries to the neck. They have been used also for the treatment of a variety of clinical conditions that have in common only the presence of skeletal muscle hyperactivity, for example, the muscle spasms that can occur in MULTIPLE SCLEROSIS. (From Smith and Reynard, Textbook of Pharmacology, 1991, p358)
A subset of GABA RECEPTORS that signal through their interaction with HETEROTRIMERIC G-PROTEINS.
A form of muscle hypertonia associated with upper MOTOR NEURON DISEASE. Resistance to passive stretch of a spastic muscle results in minimal initial resistance (a "free interval") followed by an incremental increase in muscle tone. Tone increases in proportion to the velocity of stretch. Spasticity is usually accompanied by HYPERREFLEXIA and variable degrees of MUSCLE WEAKNESS. (From Adams et al., Principles of Neurology, 6th ed, p54)
Implanted fluid propulsion systems with self-contained power source for providing long-term controlled-rate delivery of drugs such as chemotherapeutic agents or analgesics. Delivery rate may be externally controlled or osmotically or peristatically controlled with the aid of transcutaneous monitoring.
Drugs that bind to but do not activate GABA-B RECEPTORS thereby blocking the actions of endogenous or exogenous GABA-B RECEPTOR AGONISTS.
The sodium salt of 4-hydroxybutyric acid. It is used for both induction and maintenance of ANESTHESIA.
A neurotoxic isoxazole isolated from species of AMANITA. It is obtained by decarboxylation of IBOTENIC ACID. Muscimol is a potent agonist of GABA-A RECEPTORS and is used mainly as an experimental tool in animal and tissue studies.
Introduction of therapeutic agents into the spinal region using a needle and syringe.
Drugs that bind to but do not activate GABA RECEPTORS, thereby blocking the actions of endogenous GAMMA-AMINOBUTYRIC ACID and GABA RECEPTOR AGONISTS.
Inorganic or organic derivatives of phosphinic acid, H2PO(OH). They include phosphinates and phosphinic acid esters.
The most common inhibitory neurotransmitter in the central nervous system.
An isoquinoline alkaloid obtained from Dicentra cucullaria and other plants. It is a competitive antagonist for GABA-A receptors.
Cell surface proteins which bind GAMMA-AMINOBUTYRIC ACID and contain an integral membrane chloride channel. Each receptor is assembled as a pentamer from a pool of at least 19 different possible subunits. The receptors belong to a superfamily that share a common CYSTEINE loop.
Organic compounds that contain phosphorus as an integral part of the molecule. Included under this heading is broad array of synthetic compounds that are used as PESTICIDES and DRUGS.
Substances used for their pharmacological actions on GABAergic systems. GABAergic agents include agonists, antagonists, degradation or uptake inhibitors, depleters, precursors, and modulators of receptor function.
Nipecotic acids are a class of compounds, specifically GABAergic drugs, that act as reversible inhibitors of the presynaptic GABA transporter (GAT), increasing the concentration of GABA in the synaptic cleft and enhancing its inhibitory effects on neurotransmission.
The administration of medication by insertion of a tiny needle or catheter into the spinal sac or epidural cavity.
Cell-surface proteins that bind GAMMA-AMINOBUTYRIC ACID with high affinity and trigger changes that influence the behavior of cells. GABA-A receptors control chloride channels formed by the receptor complex itself. They are blocked by bicuculline and usually have modulatory sites sensitive to benzodiazepines and barbiturates. GABA-B receptors act through G-proteins on several effector systems, are insensitive to bicuculline, and have a high affinity for L-baclofen.
Amino acids with uncharged R groups or side chains.
An involuntary contraction of a muscle or group of muscles. Spasms may involve SKELETAL MUSCLE or SMOOTH MUSCLE.
Stones in the URINARY BLADDER; also known as vesical calculi, bladder stones, or cystoliths.
Endogenous compounds and drugs that bind to and activate GABA-A RECEPTORS.

Neurite outgrowth-regulating properties of GABA and the effect of serum on mouse spinal cord neurons in culture. (1/869)

Time-lapse photography was used to examine the effects of gamma-aminobutyric acid (GABA) on the outgrowth and motility of neurites in cultures from mouse spinal cord. GABA at concentrations of 100, 10 and 1 microM caused significant inhibition of neurite outgrowth and the motility of growth cones was significantly reduced by treatment with 100 and 10 microM GABA. This effect was mimicked by the GABA(B) receptor agonist baclofen, whereas the GABA(A) receptor agonist muscimol had no effect. The effect of GABA on outgrowth and motility seems to be dependent on the type of serum employed. The results reported here were obtained only when heat-inactivated serum was used and not when non heat-inactivated serum was added to the culture medium. They suggest that GABA has a role in the regulation of process outgrowth within the embryonic mouse spinal cord.  (+info)

Carbamazepine facilitates effects of GABA on rat hippocampus slices. (2/869)

AIM: To study the influence of carbamazepine (Car) on GABA effect in hippocampus. METHODS: Evoked potentials were recorded on pyramidal cells in CA1 after stimulation (0.5 Hz, 50 microseconds) to Schaffer collaterals in rat hippocampal slices (350 microns). RESULTS: Car 0.1 and 0.2 mmol.L-1 did not affect field potentials, whereas Car 0.2 mmol.L-1 plus GABA (0.1-1 mmol.L-1) gave rise to a stronger inhibition on field potentials than that of GABA alone. Bicuculline did not reverse Car facilitation on GABA inhibition on field potentials. (-)-Baclofen was more effective in inhibiting field potentials than GABA. Car 0.2 mmol.L-1 plus (-)-baclofen (1-5 mumol.L-1) brought an inhibition stronger than that of (-)-baclofen alone. CONCLUSION: Car facilitates the effects of GABA on pyramidal cells in hippocampal CA1 region, probably related to GABAB receptors.  (+info)

Tonic activation of presynaptic GABAB receptors in the opener neuromuscular junction of crayfish. (3/869)

Release of excitatory transmitter from boutons on crayfish nerve terminals was inhibited by (R,S)-baclofen, an agonist at GABAB receptors. Baclofen had no postsynaptic actions as it reduced quantal content without affecting quantal amplitude. The effect of baclofen increased with concentration producing 18% inhibition at 10 microM; EC50, 50% inhibition at 30 microM; maximal inhibition, 85% at 100 microM and higher. There was no desensitization, even with 200 or 320 microM baclofen. Phaclofen, an antagonist at GABAB receptors, competitively antagonized the inhibitory action of baclofen (KD = 50 microM, equivalent to a pA2 = 4.3 +/- 0.1). Phaclofen on its own at concentrations below 200 microM had no effect on release, whereas at 200 microM phaclofen itself increased the control level of release by 60%, as did 2-hydroxy-saclofen (200 microM), another antagonist at GABAB receptors. This increase was evidently due to antagonism of a persistent level of GABA in the synaptic cleft, since the effect was abolished by destruction of the presynaptic inhibitory fiber, using intra-axonal pronase. We conclude that presynaptic GABAB receptors, with a pharmacological profile similar to that of mammalian GABAB receptors, are involved in the control of transmitter release at the crayfish neuromuscular junction.  (+info)

Role of presynaptic L-type Ca2+ channels in GABAergic synaptic transmission in cultured hippocampal neurons. (4/869)

Using dual whole cell patch-clamp recordings of monosynaptic GABAergic inhibitory postsynaptic currents (IPSCs) in cultured rat hippocampal neurons, we have previously demonstrated posttetanic potentiation (PTP) of IPSCs. Tetanic stimulation of the GABAergic neuron leads to accumulation of Ca2+ in the presynaptic terminals. This enhances the probability of GABA-vesicle release for up to 1 min, which underlies PTP. In the present study, we have examined the effect of altering the probability of release on PTP of IPSCs. Baclofen (10 microM), which depresses presynaptic Ca2+ entry through N- and P/Q-type voltage-dependent Ca2+ channels (VDCCs), caused a threefold greater enhancement of PTP than did reducing [Ca2+]o to 1.2 mM, which causes a nonspecific reduction in Ca2+ entry. This finding prompted us to investigate whether presynaptic L-type VDCCs contribute to the Ca2+ accumulation in the boutons during spike activity. The L-type VDCC antagonist, nifedipine (10 microM), had no effect on single IPSCs evoked at 0.2 Hz but reduced the PTP evoked by a train of 40 Hz for 2 s by 60%. Another L-type VDCC antagonist, isradipine (5 microM), similarly inhibited PTP by 65%. Both L-type VDCC blockers also depressed IPSCs during the stimulation (i.e., they increased tetanic depression). The L-type VDCC "agonist" (-)BayK 8644 (4 microM) had no effect on PTP evoked by a train of 40 Hz for 2 s, which probably saturated the PTP process, but enhanced PTP evoked by a train of 1 s by 91%. In conclusion, the results indicate that L-type VDCCs do not participate in low-frequency synchronous transmitter release, but contribute to presynaptic Ca2+ accumulation during high-frequency activity. This helps maintain vesicle release during tetanic stimulation and also enhances the probability of transmitter release during the posttetanic period, which is manifest as PTP. Involvement of L-type channels in these processes represents a novel presynaptic regulatory mechanism at fast CNS synapses.  (+info)

Interactive effects of the GABABergic modulation of calcium channels and calcium-dependent potassium channels in lamprey. (5/869)

The GABAB-mediated modulation of spinal neurons in the lamprey is investigated in this study. Activation of GABAB receptors reduces calcium currents through both low- (LVA) and high-voltage activated (HVA) calcium channels, which subsequently results in the reduction of the calcium-dependent potassium (KCa) current. This in turn will reduce the peak amplitude of the afterhyperpolarization (AHP). We used the modulatory effects of GABAB receptor activation on N-methyl-D-aspartate (NMDA)-induced, TTX-resistant membrane potential oscillations as an experimental model in which to separate the effects of GABAB receptor activation on LVA calcium channels from that on KCa channels. We show experimentally and by using simulations that a direct effect on LVA calcium channels can account for the effects of GABAB receptor activation on intrinsic membrane potential oscillations to a larger extent than indirect effects mediated via KCa channels. Furthermore, by conducting experiments and simulations on intrinsic membrane potential oscillations, we find that KCa channels may be activated by calcium entering through LVA calcium channels, providing that the decay kinetics of the calcium that enters through LVA calcium channels is not as slow as the calcium entering via NMDA receptors. A combined experimental and computational analysis revealed that the LVA calcium current also contributes to neuronal firing properties.  (+info)

GABA(B) receptor-mediated stimulation of adenylyl cyclase activity in membranes of rat olfactory bulb. (6/869)

Previous studies have shown that GABA(B) receptors facilitate cyclic AMP formation in brain slices likely through an indirect mechanism involving intracellular second messengers. In the present study, we have investigated whether a positive coupling of GABA(B) receptors to adenylyl cyclase could be detected in a cell-free preparation of rat olfactory bulb, a brain region where other Gi/Go-coupled neurotransmitter receptors have been found to stimulate the cyclase activity. The GABA(B) receptor agonist (-)-baclofen significantly increased basal adenylyl cyclase activity in membranes of the granule cell and external plexiform layers, but not in the olfactory nerve-glomerular layer. The adenylyl cyclase stimulation was therefore examined in granule cell layer membranes. The (-)-baclofen stimulation (pD2=4.53) was mimicked by 3-aminopropylphosphinic acid (pD2=4.60) and GABA (pD2=3.56), but not by (+)-baclofen, 3-aminopropylphosphonic acid, muscimol and isoguvacine. The stimulatory effect was counteracted by the GABA(B) receptor antagonists CGP 35348 (pA2=4.31), CGP 55845 A (pA2=7.0) and 2-hydroxysaclofen (pKi=4.22). Phaclofen (1 mM) was inactive. The (-)-baclofen stimulation was not affected by quinacrine, indomethacin, nordihydroguaiaretic acid and staurosporine, but was completely prevented by pertussis toxin and significantly reduced by the alpha subunit of transducin, a betagamma scavenger. The betagamma subunits of transducin stimulated the cyclase activity and this effect was not additive with that produced by (-)-baclofen. In the external plexiform and granule cell layers, but not in the olfactory nerve-glomerular layer, (-)-baclofen enhanced the adenylyl cyclase stimulation elicited by the neuropeptide pituitary adenylate cyclase activating polypeptide (PACAP) 38. Conversely, the adenylyl cyclase activity stimulated by either forskolin or Ca2+/calmodulin-(Ca2+/CaM) was inhibited by (-)-baclofen in all the olfactory bulb layers examined. These data demonstrate that in specific layers of rat olfactory bulb activation of GABA(B) receptors enhances basal and neurotransmitter-stimulated adenylyl cyclase activities by a mechanism involving betagamma subunits of Gi/Go. This positive coupling is associated with a widespread inhibitory effect on forskolin- and Ca2+/CaM-stimulated cyclic AMP formation.  (+info)

Cholinergic and GABAergic regulation of nitric oxide synthesis in the guinea pig ileum. (7/869)

Nitric oxide (NO) synthesis was examined in intact longitudinal muscle-myenteric plexus preparations of the guinea pig ileum by determining the formation of [3H]citrulline during incubation with [3H]arginine. Spontaneous [3H]citrulline production after 30 min was 80-90 dpm/mg, which constituted approximately 1% of the tissue radioactivity. Electrical stimulation (10 Hz) led to a threefold increase in [3H]citrulline formation. Removal of calcium from the medium or addition of NG-nitro-L-arginine strongly inhibited both spontaneous and electrically induced production of [3H]citrulline. TTX reduced the electrically induced but not spontaneous [3H]citrulline formation. The electrically induced formation of [3H]citrulline was diminished by (+)-tubocurarine and mecamylamine and enhanced by scopolamine, which suggests that endogenous ACh inhibits, via muscarinic receptors, and stimulates, via nicotinic receptors, the NO synthesis in the myenteric plexus. The GABAA receptor agonist muscimol and GABA also reduced the electrically evoked formation of [3H]citrulline, whereas baclofen was without effect. Bicuculline antagonized the inhibitory effect of GABA. It is concluded that nitrergic myenteric neurons are equipped with GABAA receptors, which mediate inhibition of NO synthesis.  (+info)

Neuropeptide-mediated facilitation and inhibition of sensory inputs and spinal cord reflexes in the lamprey. (8/869)

The effects of neuromodulators present in the dorsal horn [tachykinins, neuropeptide Y (NPY), bombesin, and GABAB agonists] were studied on reflex responses evoked by cutaneous stimulation in the lamprey. Reflex responses were elicited in an isolated spinal cord preparation by electrical stimulation of the attached tail fin. To be able to separate modulator-induced effects at the sensory level from that at the motor or premotor level, the spinal cord was separated into three pools with Vaseline barriers. The caudal pool contained the tail fin. Neuromodulators were added to this pool to modulate sensory inputs evoked by tail fin stimulation. The middle pool contained high divalent cation or low calcium Ringer to block polysynaptic transmission and thus limit the input to the rostral pool to that from ascending axons that project through the middle pool. Ascending inputs and reflex responses were monitored by making intracellular recordings from motor neurons and extracellular recordings from ventral roots in the rostral pool. The tachykinin neuropeptide substance P, which has previously been shown to potentiate sensory input at the cellular and synaptic levels, facilitated tail fin-evoked synaptic inputs to neurons in the rostral pool and concentration dependently facilitated rostral ventral root activity. Substance P also facilitated the modulatory effects of tail fin stimulation on ongoing locomotor activity in the rostral pool. In contrast, NPY and the GABAB receptor agonist baclofen, both of which have presynaptic inhibitory effects on sensory afferents, reduced the strength of ascending inputs and rostral ventral root responses. We also examined the effects of the neuropeptide bombesin, which is present in sensory axons, at the cellular, synaptic, and reflex levels. As with substance P, bombesin increased tail fin stimulation-evoked inputs and ventral root responses in the rostral pool. These effects were associated with the increased excitability of slowly adapting mechanosensory neurons and the potentiation of glutamatergic synaptic inputs to spinobulbar neurons. These results show the possible behavioral relevance of neuropeptide-mediated modulation of sensory inputs at the cellular and synaptic levels. Given that the types and locations of neuropeptides in the dorsal spinal cord of the lamprey show strong homologies to that of higher vertebrates, these results are presumably relevant to other vertebrate systems.  (+info)

Baclofen is a muscle relaxant and antispastic medication. It is primarily used to treat spasticity, a common symptom in individuals with spinal cord injuries, multiple sclerosis, cerebral palsy, and other neurological disorders that can cause stiff and rigid muscles.

Baclofen works by reducing the activity of overactive nerves in the spinal cord that are responsible for muscle contractions. It binds to GABA-B receptors in the brain and spinal cord, increasing the inhibitory effects of gamma-aminobutyric acid (GABA), a neurotransmitter that helps regulate communication between nerve cells. This results in decreased muscle spasticity and improved range of motion.

The medication is available as an oral tablet or an injectable solution for intrathecal administration, which involves direct delivery to the spinal cord via a surgically implanted pump. The oral formulation is generally preferred as a first-line treatment due to its non-invasive nature and lower risk of side effects compared to intrathecal administration.

Common side effects of baclofen include drowsiness, weakness, dizziness, headache, and nausea. Intrathecal baclofen may cause more severe side effects, such as seizures, respiratory depression, and allergic reactions. Abrupt discontinuation of the medication can lead to withdrawal symptoms, including hallucinations, confusion, and increased muscle spasticity.

It is essential to consult a healthcare professional for personalized medical advice regarding the use and potential side effects of baclofen.

GABA-B receptor agonists are substances that bind to and activate GABA-B receptors, which are G protein-coupled receptors found in the central nervous system. GABA (gamma-aminobutyric acid) is the primary inhibitory neurotransmitter in the brain, and its activation leads to decreased neuronal excitability.

GABA-B receptor agonists can produce various effects on the body, including sedation, anxiolysis, analgesia, and anticonvulsant activity. Some examples of GABA-B receptor agonists include baclofen, gabapentin, and pregabalin. These drugs are used in the treatment of a variety of medical conditions, such as muscle spasticity, epilepsy, and neuropathic pain.

It's important to note that while GABA-B receptor agonists can have therapeutic effects, they can also produce side effects such as dizziness, weakness, and respiratory depression, especially at high doses or in overdose situations. Therefore, these drugs should be used with caution and under the supervision of a healthcare provider.

GABA (gamma-aminobutyric acid) agonists are substances that bind to and activate GABA receptors in the brain, mimicking the actions of GABA, which is the primary inhibitory neurotransmitter in the central nervous system. These agents can produce various effects such as sedation, anxiolysis, muscle relaxation, and anticonvulsant activity by enhancing the inhibitory tone in the brain. They are used clinically to treat conditions such as anxiety disorders, seizures, and muscle spasticity. Examples of GABA agonists include benzodiazepines, barbiturates, and certain non-benzodiazepine hypnotics.

Central muscle relaxants are a class of pharmaceutical agents that act on the central nervous system (CNS) to reduce skeletal muscle tone and spasticity. These medications do not directly act on the muscles themselves but rather work by altering the messages sent between the brain and the muscles, thereby reducing excessive muscle contraction and promoting relaxation.

Central muscle relaxants are often prescribed for the management of various neuromuscular disorders, such as multiple sclerosis, spinal cord injuries, cerebral palsy, and stroke-induced spasticity. They may also be used to treat acute musculoskeletal conditions like strains, sprains, or other muscle injuries.

Examples of central muscle relaxants include baclofen, tizanidine, cyclobenzaprine, methocarbamol, and diazepam. It is important to note that these medications can have side effects such as drowsiness, dizziness, and impaired cognitive function, so they should be used with caution and under the guidance of a healthcare professional.

GABA-B receptors are a type of G protein-coupled receptor that is activated by the neurotransmitter gamma-aminobutyric acid (GABA). These receptors are found throughout the central nervous system and play a role in regulating neuronal excitability. When GABA binds to GABA-B receptors, it causes a decrease in the release of excitatory neurotransmitters and an increase in the release of inhibitory neurotransmitters, which results in a overall inhibitory effect on neuronal activity. GABA-B receptors are involved in a variety of physiological processes, including the regulation of muscle tone, cardiovascular function, and pain perception. They have also been implicated in the pathophysiology of several neurological and psychiatric disorders, such as epilepsy, anxiety, and addiction.

Muscle spasticity is a motor disorder characterized by an involuntary increase in muscle tone, leading to stiffness and difficulty in moving muscles. It is often seen in people with damage to the brain or spinal cord, such as those with cerebral palsy, multiple sclerosis, or spinal cord injuries.

In muscle spasticity, the muscles may contract excessively, causing rigid limbs, awkward movements, and abnormal postures. The severity of muscle spasticity can vary from mild stiffness to severe contractures that limit mobility and function.

Muscle spasticity is caused by an imbalance between excitatory and inhibitory signals in the central nervous system, leading to overactivity of the alpha motor neurons that control muscle contraction. This can result in hyperreflexia (overactive reflexes), clonus (rapid, rhythmic muscle contractions), and flexor or extensor spasms.

Effective management of muscle spasticity may involve a combination of physical therapy, medication, surgery, or other interventions to improve function, reduce pain, and prevent complications such as contractures and pressure sores.

An implantable infusion pump is a small, programmable medical device that is surgically placed under the skin to deliver precise amounts of medication directly into the body over an extended period. These pumps are often used for long-term therapies, such as managing chronic pain, delivering chemotherapy drugs, or administering hormones for conditions like diabetes or growth hormone deficiency.

The implantable infusion pump consists of a reservoir to hold the medication and a mechanism to control the rate and timing of its delivery. The device can be refilled periodically through a small incision in the skin. Implantable infusion pumps are designed to provide consistent, controlled dosing with minimal side effects and improved quality of life compared to traditional methods like injections or oral medications.

It is important to note that implantable infusion pumps should only be used under the guidance and care of a healthcare professional, as they require careful programming and monitoring to ensure safe and effective use.

GABA-B receptor antagonists are pharmacological agents that block the activation of GABA-B receptors, which are G protein-coupled receptors found in the central and peripheral nervous systems. Gamma-aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the brain, and it exerts its effects by binding to GABA-A and GABA-B receptors.

GABA-B receptor antagonists work by preventing GABA from binding to these receptors, thereby blocking the inhibitory effects of GABA. This can lead to increased neuronal excitability and can have various pharmacological effects depending on the specific receptor subtype and location in the body.

GABA-B receptor antagonists have been investigated for their potential therapeutic use in a variety of neurological and psychiatric disorders, such as epilepsy, depression, anxiety, and substance abuse disorders. However, their clinical use is still not well established due to limited efficacy and potential side effects, including increased anxiety, agitation, and seizures.

Sodium oxybate is a central nervous system depressant, which is a sodium salt of gamma-hydroxybutyric acid (GHB). It is also known as gamma-hydroxybutyrate monosodium salt or sodium GHB. Sodium oxybate is used in the medical field for the treatment of narcolepsy, a sleep disorder characterized by excessive daytime sleepiness and cataplexy (sudden loss of muscle tone). It is sold under the brand name Xyrem.

Sodium oxybate works by affecting the neurotransmitters in the brain, specifically increasing the levels of gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter that helps regulate sleep and wakefulness. The medication is available only through a restricted distribution program due to its potential for abuse and dependence. It is usually taken at night in two doses, one at bedtime and the other about 2.5 to 4 hours later.

It's important to note that sodium oxybate has a high potential for misuse and addiction, and it should only be used under the close supervision of a healthcare provider.

Muscimol is defined as a cyclic psychoactive ingredient found in certain mushrooms, including Amanita muscaria and Amanita pantherina. It acts as a potent agonist at GABA-A receptors, which are involved in inhibitory neurotransmission in the central nervous system. Muscimol can cause symptoms such as altered consciousness, delirium, hallucinations, and seizures. It is used in research but has no medical applications.

Spinal injections, also known as epidural injections or intrathecal injections, are medical procedures involving the injection of medications directly into the spinal canal. The medication is usually delivered into the space surrounding the spinal cord (the epidural space) or into the cerebrospinal fluid that surrounds and protects the spinal cord (the subarachnoid space).

The medications used in spinal injections can include local anesthetics, steroids, opioids, or a combination of these. The purpose of spinal injections is to provide diagnostic information, therapeutic relief, or both. They are commonly used to treat various conditions affecting the spine, such as radicular pain (pain that radiates down the arms or legs), disc herniation, spinal stenosis, and degenerative disc disease.

Spinal injections can be administered using different techniques, including fluoroscopy-guided injections, computed tomography (CT) scan-guided injections, or with the help of a nerve stimulator. These techniques ensure accurate placement of the medication and minimize the risk of complications.

It is essential to consult a healthcare professional for specific information regarding spinal injections and their potential benefits and risks.

GABA (gamma-aminobutyric acid) antagonists are substances that block the action of GABA, which is the primary inhibitory neurotransmitter in the central nervous system. GABA plays a crucial role in regulating neuronal excitability and reducing the transmission of nerve impulses.

GABA antagonists work by binding to the GABA receptors without activating them, thereby preventing the normal function of GABA and increasing neuronal activity. These agents can cause excitation of the nervous system, leading to various effects depending on the specific type of GABA receptor they target.

GABA antagonists are used in medical treatments for certain conditions, such as sleep disorders, depression, and cognitive enhancement. However, they can also have adverse effects, including anxiety, agitation, seizures, and even neurotoxicity at high doses. Examples of GABA antagonists include picrotoxin, bicuculline, and flumazenil.

I'm sorry for any confusion, but "Phosphinic Acids" is not a recognized medical term. Phosphinic acids are chemical compounds that contain a phosphorus atom bonded to two organic groups and one hydroxyl group, making them a subclass of organophosphorus compounds. They are widely used in the production of various chemicals, but they do not have specific relevance to medical definitions or terminology. If you have any questions related to medicine or health, I'd be happy to try to help answer those!

Gamma-Aminobutyric Acid (GABA) is a major inhibitory neurotransmitter in the mammalian central nervous system. It plays a crucial role in regulating neuronal excitability and preventing excessive neuronal firing, which helps to maintain neural homeostasis and reduce the risk of seizures. GABA functions by binding to specific receptors (GABA-A, GABA-B, and GABA-C) on the postsynaptic membrane, leading to hyperpolarization of the neuronal membrane and reduced neurotransmitter release from presynaptic terminals.

In addition to its role in the central nervous system, GABA has also been identified as a neurotransmitter in the peripheral nervous system, where it is involved in regulating various physiological processes such as muscle relaxation, hormone secretion, and immune function.

GABA can be synthesized in neurons from glutamate, an excitatory neurotransmitter, through the action of the enzyme glutamic acid decarboxylase (GAD). Once synthesized, GABA is stored in synaptic vesicles and released into the synapse upon neuronal activation. After release, GABA can be taken up by surrounding glial cells or degraded by the enzyme GABA transaminase (GABA-T) into succinic semialdehyde, which is further metabolized to form succinate and enter the Krebs cycle for energy production.

Dysregulation of GABAergic neurotransmission has been implicated in various neurological and psychiatric disorders, including epilepsy, anxiety, depression, and sleep disturbances. Therefore, modulating GABAergic signaling through pharmacological interventions or other therapeutic approaches may offer potential benefits for the treatment of these conditions.

Bicuculline is a pharmacological agent that acts as a competitive antagonist at GABA-A receptors, which are inhibitory neurotransmitter receptors in the central nervous system. By blocking the action of GABA (gamma-aminobutyric acid) at these receptors, bicuculline can increase neuronal excitability and cause convulsions. It is used in research to study the role of GABAergic neurotransmission in various physiological processes and neurological disorders.

GABA-A receptors are ligand-gated ion channels in the membrane of neuronal cells. They are the primary mediators of fast inhibitory synaptic transmission in the central nervous system. When the neurotransmitter gamma-aminobutyric acid (GABA) binds to these receptors, it opens an ion channel that allows chloride ions to flow into the neuron, resulting in hyperpolarization of the membrane and decreased excitability of the neuron. This inhibitory effect helps to regulate neural activity and maintain a balance between excitation and inhibition in the nervous system. GABA-A receptors are composed of multiple subunits, and the specific combination of subunits can determine the receptor's properties, such as its sensitivity to different drugs or neurotransmitters.

Organophosphorus compounds are a class of chemical substances that contain phosphorus bonded to organic compounds. They are used in various applications, including as plasticizers, flame retardants, pesticides (insecticides, herbicides, and nerve gases), and solvents. In medicine, they are also used in the treatment of certain conditions such as glaucoma. However, organophosphorus compounds can be toxic to humans and animals, particularly those that affect the nervous system by inhibiting acetylcholinesterase, an enzyme that breaks down the neurotransmitter acetylcholine. Exposure to these compounds can cause symptoms such as nausea, vomiting, muscle weakness, and in severe cases, respiratory failure and death.

GABA (gamma-aminobutyric acid) agents are pharmaceutical drugs that act as agonists at the GABA receptors in the brain. GABA is the primary inhibitory neurotransmitter in the central nervous system, and it plays a crucial role in regulating neuronal excitability.

GABA agents can enhance the activity of GABA by increasing the frequency or duration of GABA-mediated chloride currents at the GABA receptors. These drugs are often used as anticonvulsants, anxiolytics, muscle relaxants, and sedatives due to their ability to reduce neuronal excitability and promote relaxation.

Examples of GABA agents include benzodiazepines, barbiturates, non-benzodiazepine hypnotics, and certain anticonvulsant drugs such as gabapentin and pregabalin. It is important to note that while these drugs can be effective in treating various medical conditions, they also carry the risk of dependence, tolerance, and adverse effects, particularly when used at high doses or for prolonged periods.

Nipecotic acids are a class of compounds that function as GABA transaminase inhibitors. GABA (gamma-aminobutyric acid) is the primary inhibitory neurotransmitter in the central nervous system, and its levels are regulated by enzymes such as GABA transaminase.

Nipecotic acids work by inhibiting this enzyme, leading to an increase in GABA levels in the brain. This can have various effects on the nervous system, including sedative, hypnotic, and anticonvulsant actions. Some nipecotic acid derivatives are used in research as tools for studying the role of GABA in the brain, while others have been investigated for their potential therapeutic uses in treating conditions such as anxiety, insomnia, and epilepsy.

It's important to note that nipecotic acids and their derivatives can have significant side effects and toxicity, and they are not approved for use as medications in most countries. Therefore, they should only be used under the close supervision of a trained medical professional for research purposes.

Spinal infusions, also known as intrathecal infusions, refer to the administration of medications directly into the spinal canal through a surgically implanted device. This device typically consists of a pump and a catheter. The pump is a small reservoir that contains the medication, while the catheter is a thin tube that delivers the medication to the intrathecal space, which is the area surrounding the spinal cord.

This route of administration is often used for the management of chronic pain, as well as for the treatment of certain neurological disorders such as spasticity and severe muscle spasms. The medications that are commonly administered through spinal infusions include local anesthetics, opioids, and muscle relaxants.

The main advantage of spinal infusions is that they allow for the delivery of medication directly to the site of action, which can result in more effective pain relief and fewer systemic side effects compared to systemic administration. However, there are also potential risks associated with this procedure, including infection, bleeding, and mechanical failure of the device. Therefore, spinal infusions should only be performed by trained medical professionals in a controlled clinical setting.

GABA (gamma-aminobutyric acid) receptors are a type of neurotransmitter receptor found in the central nervous system. They are responsible for mediating the inhibitory effects of the neurotransmitter GABA, which is the primary inhibitory neurotransmitter in the mammalian brain.

GABA receptors can be classified into two main types: GABA-A and GABA-B receptors. GABA-A receptors are ligand-gated ion channels, which means that when GABA binds to them, it opens a channel that allows chloride ions to flow into the neuron, resulting in hyperpolarization of the membrane and decreased excitability. GABA-B receptors, on the other hand, are G protein-coupled receptors that activate inhibitory G proteins, which in turn reduce the activity of calcium channels and increase the activity of potassium channels, leading to hyperpolarization of the membrane and decreased excitability.

GABA receptors play a crucial role in regulating neuronal excitability and are involved in various physiological processes such as sleep, anxiety, muscle relaxation, and seizure control. Dysfunction of GABA receptors has been implicated in several neurological and psychiatric disorders, including epilepsy, anxiety disorders, and insomnia.

Neutral amino acids are a type of amino acids that are characterized by the presence of a neutral side chain in their chemical structure. In other words, the side chain of these amino acids does not contain any ionizable groups, such as carboxyl or amino groups, which can give rise to positive or negative charges.

There are nine neutral amino acids in total, and they include:

1. Alanine (Ala) - has a methyl group (-CH3) as its side chain
2. Glycine (Gly) - has a hydrogen atom (-H) as its side chain
3. Valine (Val) - has an isopropyl group (-CH(CH3)2) as its side chain
4. Leucine (Leu) - has a branched alkyl group (-CH2CH(CH3)2) as its side chain
5. Isoleucine (Ile) - has a sec-butyl group (-CH(CH3)(CH2CH3)) as its side chain
6. Proline (Pro) - has a cyclic structure containing a secondary amino group (-NH-) as its side chain
7. Phenylalanine (Phe) - has an aromatic ring with a methyl group (-CH3) attached to it as its side chain
8. Tryptophan (Trp) - has an indole ring as its side chain
9. Methionine (Met) - has a sulfur-containing alkyl group (-CH2CH2SH) as its side chain

Neutral amino acids play important roles in various biological processes, such as protein synthesis, metabolism, and signaling pathways. They are also essential components of many dietary proteins and are required for the growth, development, and maintenance of tissues and organs in the body.

A spasm is a sudden, involuntary contraction or tightening of a muscle, group of muscles, or a hollow organ such as the ureter or bronchi. Spasms can occur as a result of various factors including muscle fatigue, injury, irritation, or abnormal nerve activity. They can cause pain and discomfort, and in some cases, interfere with normal bodily functions. For example, a spasm in the bronchi can cause difficulty breathing, while a spasm in the ureter can cause severe pain and may lead to a kidney stone blockage. The treatment for spasms depends on the underlying cause and may include medication, physical therapy, or lifestyle changes.

Urinary bladder calculi, also known as bladder stones, refer to the formation of solid mineral deposits within the urinary bladder. These calculi develop when urine becomes concentrated, allowing minerals to crystallize and stick together, forming a stone. Bladder stones can vary in size, ranging from tiny sand-like particles to larger ones that can occupy a significant portion of the bladder's volume.

Bladder stones typically form as a result of underlying urinary tract issues, such as bladder infection, enlarged prostate, nerve damage, or urinary retention. Symptoms may include lower abdominal pain, difficulty urinating, frequent urination, blood in the urine, and sudden, strong urges to urinate. If left untreated, bladder stones can lead to complications like urinary tract infections and kidney damage. Treatment usually involves surgical removal of the stones or using other minimally invasive procedures to break them up and remove the fragments.

GABA-A receptor agonists are substances that bind to and activate GABA-A receptors, which are ligand-gated ion channels found in the central nervous system. GABA (gamma-aminobutyric acid) is the primary inhibitory neurotransmitter in the brain, and its activation via GABA-A receptors results in hyperpolarization of neurons and reduced neuronal excitability.

GABA-A receptor agonists can be classified into two categories: GABAergic compounds and non-GABAergic compounds. GABAergic compounds, such as muscimol and isoguvacine, are structurally similar to GABA and directly activate the receptors. Non-GABAergic compounds, on the other hand, include benzodiazepines, barbiturates, and neurosteroids, which allosterically modulate the receptor's affinity for GABA, thereby enhancing its inhibitory effects.

These agents are used in various clinical settings to treat conditions such as anxiety, insomnia, seizures, and muscle spasticity. However, they can also produce adverse effects, including sedation, cognitive impairment, respiratory depression, and physical dependence, particularly when used at high doses or for prolonged periods.

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Baclofen oral. US National Library of Medicine (Medline) (2003-04-01). Retrieved on 2007-10-17. Dantrolene oral. US National ... Becker WJ, Harris CJ, Long ML, Ablett DP, Klein GM, DeForge DA (1995). "Long-term intrathecal baclofen therapy in patients with ... In the most complicated cases intrathecal injections of baclofen can be used. There are also palliative measures like castings ... There is evidence, albeit limited, of the clinical effectiveness of THC and CBD extracts, baclofen, dantrolene, diazepam, and ...
Development of baclofen/samidorphan has also been discontinued. Samidorphan has been investigated for the treatment of ... "Baclofen/samidorphan". Adis Insight. Springer Nature Switzerland AG. Hillemacher T, Heberlein A, Muschler MA, Bleich S, ...
Baclofen, a GABAB receptor agonist, is under study for the treatment of alcoholism. According to a 2017 Cochrane Systematic ... Leggio, L; Garbutt, JC; Addolorato, G (March 2010). "Effectiveness and safety of baclofen in the treatment of alcohol dependent ... Liu, Jia; Wang, Lu-Ning (20 August 2017). "Baclofen for alcohol withdrawal". The Cochrane Database of Systematic Reviews. 8 (8 ... Review, there is insufficient evidence to determine the effectiveness or safety for the use of baclofen for withdrawal symptoms ...
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Baclofen pumps are often used for individuals with spasticity associated with quadriplegia or paraplegia People with spastic ... For baclofen pumps, this may be once every 5-7 years. Infusion pump Intrathecal administration Medical Advisory, Secretariat ( ... "Intrathecal Baclofen Pumps Fact Sheet" (PDF). Women's and Children's Hospital. Government of South Australia. Archived from the ... Medications such as baclofen, bupivacaine, clonidine, morphine, hydromorphone, fentanyl or ziconotide may be delivered in this ...
Baclofen was first suggested as an adjunct because benzodiazepines do not affect GABAB receptors and therefore have no cross- ... However, there is less experience with the use of baclofen for GHB withdrawal, and additional research in humans is needed. ... Higher concentrations inhibit dopamine release via GABAB receptors as do other GABAB agonists such as baclofen and phenibut. ... LeTourneau JL, Hagg DS, Smith SM (2008). "Baclofen and gamma-hydroxybutyrate withdrawal". Neurocritical Care. 8 (3): 430-33. ...
Francisco GE, Hu MM, Boake C, Ivanhoe CB (May 2005). "Efficacy of early use of intrathecal baclofen therapy for treating ... Francisco GE, Saulino MF, Yablon SA, Turner M (September 2009). "Intrathecal baclofen therapy: an update". PM & R. 1 (9): 852-8 ... such as baclofen) directly to the site of action) Electrical stimulation of the nervous system has a long and complex history. ...
In a study in rats, homotaurine reversed the catatonia induced by baclofen (the prototypical GABAB agonist), and was able to ... Mehta, A; Ticku, M (September 1987). "Baclofen induces catatonia in rats". Neuropharmacology. 26 (9): 1419-1423. doi:10.1016/ ... becoming an antagonist and displacing the full agonists GABA and baclofen at this receptor. ...
In January 2022, Amneal announced it would acquire Saol Therapeutics Baclofen franchise for around $83.5 million, plus future ... ". "Amneal Acquires Saol Therapeutics' Baclofen Franchise". "Amneal And Impax Complete Business Combination". Biosimilar ...
Baclofen and tizanidine may reduce spasticity. Quinine or phenytoin may decrease cramps. Some patients who do not receive ... adequate relief from oral treatment may consider intrathecal baclofen (i.e., infusion of medication directly into the ...
... a peripheral and central baclofen antagonist". Brain Research. 405 (1): 150-154. doi:10.1016/0006-8993(87)90999-1. PMID 3032346 ...
Other GABAergic modulators include: GABAB receptor ligands.[citation needed] Agonists: baclofen, propofol, GHB, phenibut. ...
Baclofen (β-(4-chlorophenyl)-GABA) - antispasmodic drug; potent GABAB receptor agonist, weak inhibitor of α2δ subunit- ...
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Baclofen is sometimes used as an alternative to diazepam. Diazepam is marketed in over 500 brands throughout the world. It is ...
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Other options include lamotrigine, baclofen, gabapentin, amitriptyline and pimozide. Opioids are not usually effective in the ... The anticonvulsant carbamazepine is the first line treatment; second line medications include baclofen, lamotrigine, ...
Intrathecal baclofen (ITB) therapy is used to treat a variety of movement disorders such as cerebral palsy and multiple ... Francisco GE (2006). "Successful treatment of posttraumatic hemiballismus with intrathecal baclofen therapy". American Journal ...
Evidence for baclofen, botulinum toxin, and capsaicin is unclear. There are two primary treatments for acute CH: oxygen and ...
Dmitriev AV, Andreev NI (1987). "[The spectrum of analgesic activity of baclofen and tolibut]". Farmakologiia I Toksikologiia ( ... and is also an analogue of baclofen where the 4-chloro substitution has been replaced with a 4-methyl substitution. Tolibut has ... "Functional aspects of neuroprotective effects of new salts and compositions of baclofen in the convulsive syndrome caused by ...
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Medications such as baclofen, tizanidine, and dantrolene have been used. Muscarinic antagonist Parasympatholytic Phloroglucinol ... Effectiveness has not been clearly shown for metaxalone, methocarbamol, chlorzoxazone, baclofen, or dantrolene. Applicable ...
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Intrathecal baclofen therapy for the symptomatic treatment of hereditary spastic paraplegia. Clinical Neurology and ... Objective assessment of gait after intrathecal baclofen in hereditary spastic paraplegia. Journal of Neurology. 2005;252(8):991 ... Baclofen - a voluntary muscle relaxant to relax muscles and reduce tone. This can be administered orally or intrathecally. ( ... Improved Gait Performance in a Patient With Hereditary Spastic Paraplegia After a Continuous Intrathecal Baclofen Test Infusion ...
Baclofen or tizanidine are sometimes used as an alternative to benzodiazepines. Tizanidine has been found to have superior ... tolerability compared to diazepam and baclofen. Benzodiazepines are also used to treat the acute panic caused by hallucinogen ...
ISBN 978-0-203-48544-6. Struck, Terry H. (June 2002). "Jamais vu episodes in relationship to baclofen treatment: A case report ...
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  • Currently, the precise Baclofen mechanism of action is not fully known . (addictionresource.com)
  • Baclofen offers unique advantages over other muscle relaxants due to its specific mechanism of action. (canadiandenturecentres.com)
  • Compared to these alternatives, Baclofen offers unique advantages due to its specific mechanism of action. (canadiandenturecentres.com)
  • Serious side effects may occur if baclofen is rapidly stopped including seizures and rhabdomyolysis. (wikipedia.org)
  • Alcohol can make the side effects from baclofen worse. (medlineplus.gov)
  • Baclofen may cause side effects. (medlineplus.gov)
  • Side effects of baclofen can be very unpleasant and even unbearable for some users. (shafahome.org)
  • The approach is intended to require less medication and potentially fewer side effects than oral baclofen treatment. (medscape.com)
  • Use an oral syringe (measuring device) to accurately measure and take your dose of baclofen solution. (medlineplus.gov)
  • Some were given placebos and some were given baclofen, the dose increased slowly through the 16 week trial. (shafahome.org)
  • The usual initial dose of Baclofen for adults is 5 mg given three times daily. (medcostbuy.co.uk)
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  • The same team at the University to continue their research with groups of alcoholics who have not responded to traditional addiction treatment at high doses of baclofen to further study its efficacy. (shafahome.org)
  • Symptoms may persist even after the point at which serum baclofen levels are undetectable. (wikipedia.org)
  • The aim of the study was to assess the effect of acute (one day) and chronic (four weeks) administration of baclofen on 24 hour pH metry and symptoms in GORD patients and normal controls. (bmj.com)
  • When given for one month to GORD patients, baclofen reduces oesophageal acid refluxes and significantly improves symptoms. (bmj.com)
  • Baclofen is primarily used to manage muscle symptoms associated with neurological disorders. (canadiandenturecentres.com)
  • Baclofen is primarily used for the treatment of spastic movement disorders, especially in instances of spinal cord injury, cerebral palsy, and multiple sclerosis. (wikipedia.org)
  • Lioresal (Baclofen) treats muscle spasms caused by multiple sclerosis, cerebral palsy, or damage to the brain or spinal cord. (blessedpharmacy.com)
  • Baclofen can also be prescribed for individuals with cerebral palsy, a neurological disorder often characterized by involuntary muscle movements. (canadiandenturecentres.com)
  • A presumptive diagnosis of baclofen toxicity was made, and the patient underwent continuous hemodialysis sessions, leading to neurological recovery within two days. (bvsalud.org)
  • Baclofen acts on the spinal cord nerves and decreases the number and severity of muscle spasms caused by multiple sclerosis or spinal cord conditions. (medlineplus.gov)
  • Baclofen is used to treat muscle spasms caused by certain conditions (such as multiple sclerosis, spinal cord injury/disease). (blessedpharmacy.com)
  • Baclofen is used for the treatment of muscle spasms, caused by multiple sclerosis and other diseases. (canadian-rxpharmacy.com)
  • Baclofen is used for treating spasm of skeletal muscles, muscle clonus, cramping of muscles, rigidity, spinal cord injury and pain caused by disorders such as multiple sclerosis. (medcostbuy.co.uk)
  • While traditional muscle relaxants tend to act on the muscles directly, Baclofen primarily targets the central nervous system, specifically the Gamma-Aminobutyric Acid (GABA) receptors. (canadiandenturecentres.com)
  • Baclofen acts by relaxing skeletal muscles, the muscles that move the skeleton (and also called striated muscle). (medcostbuy.co.uk)
  • Chemically, baclofen is a derivative of the neurotransmitter γ-aminobutyric acid (GABA). (wikipedia.org)
  • Baclofen specifically binds to GABA-B receptors, leading to hyperpolarization and inhibition of neurotransmitter release, thereby reducing muscle spasms and rigidity. (canadiandenturecentres.com)
  • The adverse effects and safety profile associated with baclofen when it is combined with sedative drugs (for example alcohol or benzodiazepines) are unknown. (wikipedia.org)
  • These effects might get worse if you take Baclofen with alcohol or specific drugs. (canadian-rxpharmacy.com)
  • Before taking Baclofen, tell your doctor about your allergy to any other drugs. (medcostbuy.co.uk)
  • Use of Baclofen with other drugs may lead to additional reduction in brain function. (medcostbuy.co.uk)
  • Acute study: 28 patients with GORD with none or mild oesophagitis at endoscopy and 15 controls underwent oesophageal and gastric 48 hour pH metry in which baclofen or placebo was given for 24 hours in a double blinded manner. (bmj.com)
  • Chronic study: 16 GORD patients received baclofen (10 mg four times daily) or placebo for four weeks. (bmj.com)
  • While more than half the patients reported significant reduction in alcohol use, it is not possible to draw definite conclusions about the effectiveness of baclofen, given that it was combined with other psychiatric and alcohol treatments, and because there was no control or comparison group. (shafahome.org)
  • Patients with an allergy to Baclofen should not take it. (medcostbuy.co.uk)
  • Baclofen toxicity is a significant concern, particularly in patients with advanced chronic kidney disease . (bvsalud.org)
  • This case highlights the risk of baclofen toxicity in dialysis -dependent patients with advanced chronic kidney disease , emphasizing the importance of vigilance and alternative treatment options in this population . (bvsalud.org)
  • According to the Baclofen MOA, it reduces the level of activity of the monosynaptic and polysynaptic reflex transmission by various actions, similar to some alternatives, and by the simulation of GABA-B receptors. (addictionresource.com)
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  • The effect of baclofen on the hind limb flexor reflex of the spinal rat. (supp.ai)
  • Another study, published in 2011, included 21 participants of which some were treated with baclofen and others given a placebo. (shafahome.org)
  • Until more research has been done on the efficacy of baclofen for treating alcoholism, it remains that the most successful method of addiction treatment is psychotherapy, especially when combined with other styles of complementary therapies. (shafahome.org)
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  • In addition to these primary medical conditions, Baclofen may be used off-label for the treatment of other conditions such as chronic hiccups and trigeminal neuralgia, a painful condition affecting the facial nerves. (canadiandenturecentres.com)
  • Baclofen, at standard dosing, does not appear to possess addictive properties, and has not been associated with any degree of drug craving. (wikipedia.org)
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  • Researchers announced that a drug called baclofen was indeed effective in treating alcoholism. (shafahome.org)
  • Baclofen may be a relatively new name in the world of addiction treatment, but it is not actually a new drug. (shafahome.org)
  • And finally, does Baclofen show up on a drug test? (addictionresource.com)
  • According to Baclofen MOA studies, and reviews from users, improvement starts to show from two days to two weeks of the initial prescription time as long as the patient continuously follows the treatment plan. (addictionresource.com)
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  • Read the Patient Information Leaflet if available from your pharmacist before you start taking baclofen and each time you get a refill. (blessedpharmacy.com)
  • pregnancy and breast feeding: contact your doctor in case if you got pregnant to discuss advantages and risks of Baclofen usage during pregnancy. (canadian-rxpharmacy.com)
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  • If you become pregnant while taking baclofen, call your doctor immediately. (medlineplus.gov)
  • Baclofen half-life is the term used to denote the time taken for half the amount of a specific medication to be removed from the body. (addictionresource.com)
  • Baclofen is also used in the treatment of sleep-related painful erections. (wikipedia.org)
  • Baclofen is sometimes used off-label as a treatment for alcohol use disorder to reduce the risk of relapse and to increase the number of days that a person can go without drinking alcohol (abstinence days). (wikipedia.org)
  • ask your doctor about the safe use of alcoholic beverages while you are taking baclofen. (medlineplus.gov)
  • While baclofen has not exactly claimed to cure alcoholism, reducing cravings is certainly be very helpful, as any recovering alcoholic would surely attest. (shafahome.org)
  • Do not stop taking baclofen without talking to your doctor, especially if you have taken large doses for a long time. (medlineplus.gov)
  • Consult with your doctor on any questions you have about Baclofen application. (canadian-rxpharmacy.com)
  • Various studies have been done on the effects of using baclofen to treat alcoholism, but the results are not exactly clear. (shafahome.org)
  • There have been several studies done on the effects of using baclofen to treat alcoholism. (shafahome.org)
  • For example, one can be prescribed Baclofen 10 mg three times a day but won't feel the effects for days. (addictionresource.com)
  • Biochemical effects of baclofen (beta-parachlorophenyl-GABA) on the dopamine and the noradrenaline in the rat brain. (supp.ai)

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