amphetamine has been researched along with Stroke in 21 studies
Amphetamine: A powerful central nervous system stimulant and sympathomimetic. Amphetamine has multiple mechanisms of action including blocking uptake of adrenergics and dopamine, stimulation of release of monamines, and inhibiting monoamine oxidase. Amphetamine is also a drug of abuse and a psychotomimetic. The l- and the d,l-forms are included here. The l-form has less central nervous system activity but stronger cardiovascular effects. The d-form is DEXTROAMPHETAMINE.
1-phenylpropan-2-amine : A primary amine that is isopropylamine in which a hydrogen attached to one of the methyl groups has been replaced by a phenyl group.
amphetamine : A racemate comprising equimolar amounts of (R)-amphetamine (also known as levamphetamine or levoamphetamine) and (S)-amphetamine (also known as dexamfetamine or dextroamphetamine.
Stroke: A group of pathological conditions characterized by sudden, non-convulsive loss of neurological function due to BRAIN ISCHEMIA or INTRACRANIAL HEMORRHAGES. Stroke is classified by the type of tissue NECROSIS, such as the anatomic location, vasculature involved, etiology, age of the affected individual, and hemorrhagic vs. non-hemorrhagic nature. (From Adams et al., Principles of Neurology, 6th ed, pp777-810)
| Excerpt | Relevance | Reference |
|---|---|---|
| "To assess the effects of d-amphetamine on motor facilitation and recovery in stroke patients with mild arm paresis receiving the Arm Ability training." | 9.11 | Amphetamine fails to facilitate motor performance and to enhance motor recovery among stroke patients with mild arm paresis: interim analysis and termination of a double blind, randomised, placebo-controlled trial. ( Eickhof, C; Engel, U; Kim, IH; Kutzner, M; Pinkowski, C; Platz, T, 2005) |
| "Neuromodulation with pharmacological agents, including drugs of abuse such as amphetamine, when paired with behavioral experience, has been shown to positively modify outcomes in animal models of stroke." | 8.93 | Amphetamine and other pharmacological agents in human and animal studies of recovery from stroke. ( Johnson, M; Mehta, J; Smith, P; Walker-Batson, D, 2016) |
| " Amphetamine can improve outcome in experimental models of stroke, and several small clinical trials have assessed its use in stroke." | 8.85 | Speeding stroke recovery? A systematic review of amphetamine after stroke. ( Bath, PM; Sprigg, N, 2009) |
| "Previously we have shown that addition of amphetamine to physical therapy results in enhanced motor improvement following stroke in rats, which was associated with the formation of new motor pathways from cortical projection neurons of the contralesional cortex." | 7.80 | Evidence for fibroblast growth factor-2 as a mediator of amphetamine-enhanced motor improvement following stroke. ( Farrer, RG; Kartje, GL; Martin, JL; Wolf, WA, 2014) |
| "The objective of this study was to examine the effects of d-amphetamine (amph) upon recovery after embolic stroke in rats." | 7.77 | Acute but not delayed amphetamine treatment improves behavioral outcome in a rat embolic stroke model. ( Johansen, FF; Kristiansen, U; Overgaard, K; Rasmussen, RS, 2011) |
| "Amphetamine (AMPH) has been proposed as a treatment for post-stroke motor deficits when coupled with symptom-relevant physical rehabilitation." | 7.74 | No improvement by amphetamine on learned non-use, attempts, success or movement in skilled reaching by the rat after motor cortex stroke. ( Alaverdashvili, M; Lim, DH; Whishaw, IQ, 2007) |
| "The dopamine-releasing and depleting substance amphetamine (AMPH) can make cortical neurons susceptible to damage, and the prevention of hyperthermia, seizures and stroke is thought to block these effects." | 7.71 | Parvalbumin neuron circuits and microglia in three dopamine-poor cortical regions remain sensitive to amphetamine exposure in the absence of hyperthermia, seizure and stroke. ( Bowyer, JF; Jakab, RL, 2002) |
| "Amphetamine-treated patients did not show any increase in motor function or ADL as compared to the control group." | 6.70 | A double-blind placebo-controlled study of the effects of amphetamine and physiotherapy after stroke. ( Lökk, J; Nilsson, CG; Nordström, M; Sonde, L; Viitanen, M, 2001) |
| "Amphetamine (AM) treatment has been shown to alter behavioral recovery after ischemia caused by embolism, permanent unilateral occlusion of the common carotid and middle cerebral arteries, or unilateral sensorimotor cortex ablation in rats." | 5.37 | Post-treatment with amphetamine enhances reinnervation of the ipsilateral side cortex in stroke rats. ( Castillo, P; Harvey, BK; Liu, HS; Lu, H; Shen, H; Wang, Y; Yang, Y, 2011) |
| "To assess the effects of d-amphetamine on motor facilitation and recovery in stroke patients with mild arm paresis receiving the Arm Ability training." | 5.11 | Amphetamine fails to facilitate motor performance and to enhance motor recovery among stroke patients with mild arm paresis: interim analysis and termination of a double blind, randomised, placebo-controlled trial. ( Eickhof, C; Engel, U; Kim, IH; Kutzner, M; Pinkowski, C; Platz, T, 2005) |
| "Neuromodulation with pharmacological agents, including drugs of abuse such as amphetamine, when paired with behavioral experience, has been shown to positively modify outcomes in animal models of stroke." | 4.93 | Amphetamine and other pharmacological agents in human and animal studies of recovery from stroke. ( Johnson, M; Mehta, J; Smith, P; Walker-Batson, D, 2016) |
| " Amphetamine can improve outcome in experimental models of stroke, and several small clinical trials have assessed its use in stroke." | 4.85 | Speeding stroke recovery? A systematic review of amphetamine after stroke. ( Bath, PM; Sprigg, N, 2009) |
| "Pharmacotherapy of aphasia had been discussed for the last twenty years with first bromocriptine and amphetamine and then serotoninergic, GABAergic and cholinergic agents." | 4.84 | Pharmacotherapy of aphasia: myth or reality? ( de Boissezon, X; de Boysson, C; Démonet, JF; Peran, P, 2007) |
| "Previously we have shown that addition of amphetamine to physical therapy results in enhanced motor improvement following stroke in rats, which was associated with the formation of new motor pathways from cortical projection neurons of the contralesional cortex." | 3.80 | Evidence for fibroblast growth factor-2 as a mediator of amphetamine-enhanced motor improvement following stroke. ( Farrer, RG; Kartje, GL; Martin, JL; Wolf, WA, 2014) |
| "The objective of this study was to examine the effects of d-amphetamine (amph) upon recovery after embolic stroke in rats." | 3.77 | Acute but not delayed amphetamine treatment improves behavioral outcome in a rat embolic stroke model. ( Johansen, FF; Kristiansen, U; Overgaard, K; Rasmussen, RS, 2011) |
| "Amphetamine (AMPH) has been proposed as a treatment for post-stroke motor deficits when coupled with symptom-relevant physical rehabilitation." | 3.74 | No improvement by amphetamine on learned non-use, attempts, success or movement in skilled reaching by the rat after motor cortex stroke. ( Alaverdashvili, M; Lim, DH; Whishaw, IQ, 2007) |
| "The dopamine-releasing and depleting substance amphetamine (AMPH) can make cortical neurons susceptible to damage, and the prevention of hyperthermia, seizures and stroke is thought to block these effects." | 3.71 | Parvalbumin neuron circuits and microglia in three dopamine-poor cortical regions remain sensitive to amphetamine exposure in the absence of hyperthermia, seizure and stroke. ( Bowyer, JF; Jakab, RL, 2002) |
| "Amphetamine-treated patients did not show any increase in motor function or ADL as compared to the control group." | 2.70 | A double-blind placebo-controlled study of the effects of amphetamine and physiotherapy after stroke. ( Lökk, J; Nilsson, CG; Nordström, M; Sonde, L; Viitanen, M, 2001) |
| "In laboratory studies, the effect of amphetamine on recovery depends on the location and extent of brain injury, the dosing and timing of amphetamine, and the type, intensity, and timing of concomitant behavioral training." | 2.45 | Amphetamine trials and tribulations. ( Goldstein, LB, 2009) |
| "Amphetamine (AM) treatment has been shown to alter behavioral recovery after ischemia caused by embolism, permanent unilateral occlusion of the common carotid and middle cerebral arteries, or unilateral sensorimotor cortex ablation in rats." | 1.37 | Post-treatment with amphetamine enhances reinnervation of the ipsilateral side cortex in stroke rats. ( Castillo, P; Harvey, BK; Liu, HS; Lu, H; Shen, H; Wang, Y; Yang, Y, 2011) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 1 (4.76) | 18.2507 |
| 2000's | 14 (66.67) | 29.6817 |
| 2010's | 6 (28.57) | 24.3611 |
| 2020's | 0 (0.00) | 2.80 |
| Authors | Studies |
|---|---|
| Lappin, JM | 1 |
| Sara, GE | 1 |
| Wolf, WA | 1 |
| Martin, JL | 1 |
| Kartje, GL | 1 |
| Farrer, RG | 1 |
| Walker-Batson, D | 2 |
| Mehta, J | 1 |
| Smith, P | 1 |
| Johnson, M | 1 |
| Goldstein, LB | 1 |
| Sprigg, N | 2 |
| Bath, PM | 2 |
| Liu, HS | 1 |
| Shen, H | 1 |
| Harvey, BK | 1 |
| Castillo, P | 1 |
| Lu, H | 1 |
| Yang, Y | 1 |
| Wang, Y | 1 |
| Rasmussen, RS | 1 |
| Overgaard, K | 1 |
| Kristiansen, U | 1 |
| Johansen, FF | 1 |
| Ali, WM | 1 |
| Al Habib, KF | 1 |
| Al-Motarreb, A | 1 |
| Singh, R | 1 |
| Hersi, A | 1 |
| Al Faleh, H | 1 |
| Asaad, N | 1 |
| Al Saif, S | 1 |
| Almahmeed, W | 1 |
| Sulaiman, K | 1 |
| Amin, H | 1 |
| Al-Lawati, J | 1 |
| Al Bustani, N | 1 |
| Al-Sagheer, NQ | 1 |
| Al-Qahtani, A | 1 |
| Al Suwaidi, J | 1 |
| Jakab, RL | 1 |
| Bowyer, JF | 1 |
| Treig, T | 1 |
| Werner, C | 1 |
| Sachse, M | 1 |
| Hesse, S | 1 |
| Brown, AW | 1 |
| Bjelke, B | 1 |
| Fuxe, K | 1 |
| Bakheit, AM | 2 |
| Gilmour, G | 1 |
| Iversen, SD | 1 |
| O'Neill, MF | 1 |
| O'Neill, MJ | 1 |
| Ward, MA | 1 |
| Bannerman, DM | 1 |
| Platz, T | 1 |
| Kim, IH | 1 |
| Engel, U | 1 |
| Pinkowski, C | 1 |
| Eickhof, C | 1 |
| Kutzner, M | 1 |
| de Boissezon, X | 1 |
| Peran, P | 1 |
| de Boysson, C | 1 |
| Démonet, JF | 1 |
| Willmot, MR | 1 |
| Gray, LJ | 1 |
| Sunderland, A | 1 |
| Pomeroy, V | 1 |
| Walker, M | 1 |
| Alaverdashvili, M | 1 |
| Lim, DH | 1 |
| Whishaw, IQ | 1 |
| Unwin, H | 1 |
| Veizovic, T | 1 |
| Beech, JS | 1 |
| Stroemer, RP | 1 |
| Watson, WP | 1 |
| Hodges, H | 1 |
| Sonde, L | 1 |
| Nordström, M | 1 |
| Nilsson, CG | 1 |
| Lökk, J | 1 |
| Viitanen, M | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Effect of Serotonin and Levodopa Functional Recovery in Patients With Cerebral Infarction[NCT02386475] | Phase 4 | 39 participants (Actual) | Interventional | 2015-01-31 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
6 reviews available for amphetamine and Stroke
| Article | Year |
|---|---|
Psychostimulant use and the brain.
Topics: Amphetamine; Amphetamine-Related Disorders; Brain; Central Nervous System Stimulants; Cocaine; Cocai | 2019 |
Amphetamine and other pharmacological agents in human and animal studies of recovery from stroke.
Topics: Amphetamine; Animals; Aphasia; Humans; Neuroprotective Agents; Recovery of Function; Stroke | 2016 |
Amphetamine trials and tribulations.
Topics: Amphetamine; Animals; Central Nervous System Stimulants; Disease Models, Animal; Dose-Response Relat | 2009 |
Speeding stroke recovery? A systematic review of amphetamine after stroke.
Topics: Amphetamine; Blood Pressure; Heart Rate; Humans; Movement Disorders; Stroke; Treatment Outcome | 2009 |
Drug treatment of poststroke aphasia.
Topics: Amphetamine; Aphasia; Bromocriptine; Humans; Stroke | 2004 |
Pharmacotherapy of aphasia: myth or reality?
Topics: Amphetamine; Aphasia; Bromocriptine; Cholinesterase Inhibitors; Clinical Trials as Topic; Donepezil; | 2007 |
5 trials available for amphetamine and Stroke
| Article | Year |
|---|---|
No benefit from D-amphetamine when added to physiotherapy after stroke: a randomized, placebo-controlled study.
Topics: Activities of Daily Living; Amphetamine; Central Nervous System Stimulants; Female; Humans; Male; Mi | 2003 |
Amphetamine fails to facilitate motor performance and to enhance motor recovery among stroke patients with mild arm paresis: interim analysis and termination of a double blind, randomised, placebo-controlled trial.
Topics: Aged; Amphetamine; Analysis of Variance; Cardiovascular System; Case-Control Studies; Central Nervou | 2005 |
Amphetamine increases blood pressure and heart rate but has no effect on motor recovery or cerebral haemodynamics in ischaemic stroke: a randomized controlled trial (ISRCTN 36285333).
Topics: Adult; Aged; Amphetamine; Blood Pressure; Brain Ischemia; Cerebrovascular Circulation; Double-Blind | 2007 |
No side effects after low-dose amphetamine administration in stroke rehabilitation.
Topics: Amphetamine; Central Nervous System Stimulants; Female; Humans; Male; Middle Aged; Stroke; Stroke Re | 2000 |
A double-blind placebo-controlled study of the effects of amphetamine and physiotherapy after stroke.
Topics: Activities of Daily Living; Administration, Oral; Aged; Aged, 80 and over; Amphetamine; Double-Blind | 2001 |
10 other studies available for amphetamine and Stroke
| Article | Year |
|---|---|
Evidence for fibroblast growth factor-2 as a mediator of amphetamine-enhanced motor improvement following stroke.
Topics: Adrenergic Agonists; Amphetamine; Animals; Axons; Fibroblast Growth Factor 2; Male; Motor Activity; | 2014 |
Post-treatment with amphetamine enhances reinnervation of the ipsilateral side cortex in stroke rats.
Topics: Amphetamine; Animals; Blotting, Western; Central Nervous System Stimulants; Cerebral Cortex; Diffusi | 2011 |
Acute but not delayed amphetamine treatment improves behavioral outcome in a rat embolic stroke model.
Topics: Amphetamine; Animals; Central Nervous System Stimulants; Disease Models, Animal; Drug Administration | 2011 |
Acute coronary syndrome and khat herbal amphetamine use: an observational report.
Topics: Acute Coronary Syndrome; Adult; Aged; Amphetamine; Catha; Female; Heart Failure; Humans; Incidence; | 2011 |
Parvalbumin neuron circuits and microglia in three dopamine-poor cortical regions remain sensitive to amphetamine exposure in the absence of hyperthermia, seizure and stroke.
Topics: Amphetamine; Animals; Astrocytes; Cerebral Cortex; Dopamine; Drug Residues; Fever; Glial Fibrillary | 2002 |
Motor response to amphetamine treatment, task-specific training, and limited motor experience in a postacute animal stroke model.
Topics: Amphetamine; Animals; Central Nervous System Stimulants; Disease Models, Animal; Disease Progression | 2004 |
Amphetamine promotes task-dependent recovery following focal cortical ischaemic lesions in the rat.
Topics: Amphetamine; Analysis of Variance; Animals; Brain Injuries; Brain Ischemia; Central Nervous System S | 2005 |
No improvement by amphetamine on learned non-use, attempts, success or movement in skilled reaching by the rat after motor cortex stroke.
Topics: Amphetamine; Analysis of Variance; Animals; Behavior, Animal; Conditioning, Operant; Disease Models, | 2007 |
Intracerebral haemorrhage in previously healthy young adults.
Topics: Adult; Amphetamine; Central Nervous System Stimulants; Cerebral Hemorrhage; Chemical and Drug Induce | 1999 |
Resolution of stroke deficits following contralateral grafts of conditionally immortal neuroepithelial stem cells.
Topics: Amphetamine; Animals; Apomorphine; Behavior, Animal; Cell Differentiation; Cell Line, Transformed; D | 2001 |