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PubMedDate not supplied

Intersubject variability of near-infrared spectroscopy signals during sensorimotor cortex activation.

We investigate the intersubject signal variability of near-infrared spectroscopy (NIRS), which is commonly used for noninvasive measurement of the product of the optical path length and the concentration change in oxygenated hemoglobin (DeltaC'oxy) and deoxygenated hemoglobin (DeltaC'deoxy) and their sum (DeltaC'total) related to human cortical activation. We do this by measuring sensorimotor cortex activation in 31 healthy adults using 24-measurement-position near-infrared (NIR) topography. A finger-tapping task is used to activate the sensorimotor cortex, and significant changes in the hemisphere contralateral to the tapping hand are assessed as being due to the activation. Of the possible patterns of signal changes, 90% include a positive DeltaC'oxy, 76% included a negative DeltaC'deoxy, and 73% included a positive DeltaC'total. The DeltaC'deoxy and DeltaC'total are less consistent because of a large intersubject variability in DeltaC'deoxy; in some cases there is a positive DeltaC'deoxy. In the cases with no positive DeltaC'oxy in the contralateral hemisphere, there are cases of other possible changes for either or both hemispheres and no cases of no change in any hemoglobin species in either hemisphere. These results suggest that NIR topography is useful for observing brain activity in most cases, although intersubject signal variability still needs to be resolved.

Adult↗

PubMed1992

Post-lesion administration of the NMDA receptor antagonist MK-801 does not impair motor recovery after unilateral sensorimotor cortex injury in the rat.

Although treatment with N-methyl-D-aspartate (NMDA) receptor antagonists reduce neuronal loss after cerebral infarction and brain trauma in laboratory animals, there is little data concerning the effects of these drugs on behavioral recovery. Because NMDA receptor antagonists impede certain kinds of learning, and because motor recovery after sensorimotor cortex injury in the rat is dependent on post-lesion experience, we hypothesized that treatment with MK-801 after focal brain injury would be detrimental. Groups of rats were first trained to traverse a narrow elevated beam and then subjected a right sensorimotor cortex suction-ablation lesion. In the first experiment, 24 h later, each rat received a single dose of either saline or the NMDA receptor antagonist MK-801 (0.5, 1.0, or 2.0 mg/kg). Beam-walking recovery was measured over the next 12 days. In a second experiment, rats were given 3 doses of MK-801 (0.5 mg/kg) at 24 h intervals beginning 24 h after cortex injury. In a third experiment, lesioned and sham-operated rats were allowed to recover for 12 days and then given MK-801 (0.5 mg/kg). Despite obvious behavioral effects of the drug, there was no overall difference in beam-walking performances among the treatment groups in any of the experiments. If 're-learning' is involved in motor recovery after cortex injury, the present results suggest that the process is not susceptible to permanent disruption by the early or late administration of an NMDA receptor antagonist.

Animals↗

PubMed2004

Sensorimotor cortex excitability in Unverricht-Lundborg disease and Lafora body disease.

OBJECTIVE: To investigate whether Unverricht-Lundborg disease (ULD) and Lafora body disease (LBD) can be differentiated on the basis of their neurophysiologic profiles. METHODS: Somatosensory evoked potentials (SSEPs), long-loop reflexes (LLRs), and the influence of conditioning nerve stimulation on the motor potentials evoked by transcranial stimulation in 8 patients with LBD and 10 patients with ULD were investigated. RESULTS: Both groups showed sensorimotor cortex hyperexcitability, but their electrophysiologic profiles were different. Enlarged P25 to N33 SSEP components and enhanced LLRs were common in the ULD patients, whereas medium-latency "giant" SSEP components and less consistently enhanced LLRs were more frequently found in the patients with LBD. Cortical relay time was extremely brief in ULD but varied in LBD. Conditioning somatosensory stimuli differently affected motor cortex excitability, leading to early facilitation in ULD and delayed and prolonged facilitation in LBD. CONCLUSIONS: Patients with Unverricht-Lundborg disease (ULD) and Lafora body disease (LBD) have different electrophysiologic profiles. The ULD findings point to an aberrant subcortical or cortical loop (possibly short-cutting the somatosensory cortex) that is involved in generating the prominent action myoclonus characterizing the disorder. The LBD findings highlight sustained hyperexcitability of the sensorimotor cortex in response to afferent stimuli, which fit with a more severe impairment of inhibitory mechanisms.

Adolescent↗

PubMed1992

The paradoxical effect of NMDA receptor stimulation on electrical activity of the sensorimotor cortex in freely behaving rats: analysis by combined EEG-intracerebral microdialysis.

This study was designed to determine the effects of N-methyl-D-aspartate (NMDA) receptor stimulation on the electrical activity of neocortex in freely behaving rats. Electroencephalogram (EEG) recording and intracerebral microdialysis were conducted simultaneously in the same site of the sensorimotor cortex, where the basal extracellular concentrations of aspartate and glutamate were 2.1 +/- 0.7 microM and 11.5 +/- 2.4 microM, respectively. Microdialysis with NMDA solutions (ranging from 10.0 microM to 10.0 mM) reduced the amplitude of the EEG activity and decreased the power of all frequency bands, with a virtual elimination of the high frequency waves, in a dose-dependent manner. These EEG changes were reversed after washing out the drug from the microdialysis fluid, and could be effectively antagonized with the competitive NMDA receptor antagonist DL-2-amino-5-phosphonovalerate. Remarkably, the NMDA actions were not associated with epileptiform behavioral or electrographic events. Control studies demonstrated that in the same experimental conditions, cholinergic receptor agonist carbachol caused seizures, and microdialysis with NMDA in the hippocampus readily induced epileptiform spikes. Our study shows that NMDA receptor stimulation in the rat sensorimotor cortex, although excitatory at synaptic level, can depress the local EEG activity. This may indicate that the NMDA receptor-mediated signals are processed by the neocortical network in a different way than by many other brain circuitries including hippocampus.

2-Amino-5-phosphonovalerate↗

PubMed2005

Rapid modulation of GABA concentration in human sensorimotor cortex during motor learning.

Movement representations within the human primary motor and somatosensory cortices can be altered by motor learning. Decreases in local GABA concentration and its release may facilitate this plasticity. Here we use in vivo magnetic resonance spectroscopy (MRS) to noninvasively measure serial changes in GABA concentration in humans in a brain region including the primary sensorimotor cortex contralateral to the hand used for an isometric motor sequence learning task. Thirty minutes of motor sequence learning reduced the mean GABA concentration within a 2 x 2 x 2-cm3 voxel by almost 20%. This reduction was specific to motor learning: 30 min of similar, movements with an unlearnable, nonrepetitive sequence were not associated with changes in GABA concentration. No significant changes in GABA concentration were found in the primary sensorimotor cortex ipsilateral to the hand used for learning. These changes suggest remarkably rapid, regionally specific short-term presynaptic modulation of GABAergic input that should facilitate motor learning. Although apparently confined to the contralateral hemisphere, the magnitude of changes seen within a large spectroscopic voxel suggests that these changes occur over a wide local neocortical field.

Adult↗

PubMed1999

Age but not sex affects motor recovery after unilateral sensorimotor cortex suction-ablation in the rat.

Both age and sex can influence recovery after brain injury. To determine the impact of these variables on motor recovery, young (2 month old) and older (5-6 months old) male and female rats were first trained to traverse a narrow elevated beam. Rats then underwent suction-ablation of right sensorimotor cortex or sham operation. Motor recovery was measured by repeated testing on the beam over 3 weeks. Shamoperated rats performed perfectly regardless of age or sex throughout testing. There was no difference in beam-walking scores among the groups of lesioned rats on the first trial 24 hrs. after injury (Kruskal-Wallis H = 0.18, p = 0.98). There was a significant effect of age (two-way ANOVA F1,32 = 29.58, p < 0.0001) but not sex (ANOVA F1,32 = 0.78, p = 0.38) on subsequent recovery. These data show that motor recovery after unilateral injury to the sensorimotor cortex varies with age, but not sex.

Journal Article↗

PubMed1990

Clonidine impairs recovery of beam-walking after a sensorimotor cortex lesion in the rat.

Beam-walking in the rat is a useful model for studying the effects of drugs on motor recovery following brain injury. In the present experiment, the effect of clonidine HCl on beam-walking recovery was investigated. Groups of rats were first trained to traverse a narrow elevated beam and then subjected to a right sensorimotor cortex suction-ablation injury. After 24 h, each rat received a single dose of clonidine HCl (20, 60, or 200 micrograms/kg, i.p., salt weight) or saline. Recovery of beam-walking ability was scored over the next 12 days. Treatment with clonidine significantly slowed the rate of recovery (Kruskal-Wallis H = 8.755, df = 3; 0.02 less than P less than 0.05). Furthermore, the impairment persisted for at least 5 days after the rats were treated (Kruskal-Wallis H = 8.47, df = 3; 0.02 less than P less than 0.05). These data are consistent with the hypothesis that norepinephrine, working through central alpha 2-adrenergic receptors, influences motor recovery after a unilateral sensorimotor cortex lesion in the rat. Since many stroke patients are treated with centrally acting antihypertensive drugs, the potential effects of specific classes of these drugs during the recovery period, should be carefully considered.

Animals↗

PubMed1995

Course and collaterals of corticospinal fibers arising from the sensorimotor cortex of the reeler mouse.

The reeler genetic mutation, occurring spontaneously in mice, affects migration of neuroblasts in the central nervous system at its last stage, causing severe cytoarchitectonic abnormalities in laminated structures, such as the cerebral and cerebellar cortex. In the reeler mouse, corticospinal (CS) neurons are malpositioned in association with the deranged laminar cytoarchitecture. To examine whether CS projections in the reeler mouse and their collaterals terminating with subcortical nuclei are normal or not, 5% biocytin was injected into the sensorimotor cortex of 2-month-old normal and reeler mice. Anterogradely labeled CS fibers of normal and reeler mice exited from the cortex and entered the internal capsule and the cerebral peduncle. They penetrated the basal pontine gray matter as longitudinal pontine fibers and entered the medullary pyramid. They continued caudally as a compact bundle along the ventral surface of the medulla, passed through the pyramidal decussation at the spinomedullary junction and entered the contralateral dorsal funiculus of the spinal cord. Both in normal and reeler mice, collaterals arising from these CS fibers projected to the ipsilateral red nucleus, basal pontine gray matter, inferior olivary complex, and the contralateral gracile nucleus. Thus, in the reeler mouse, the course and termination of CS fibers and their collaterals are identical to their normal counterparts, suggesting that radially malpositioned CS neurons in the sensorimotor cortex project to the subcortical nuclei in a manner similar to normal CS neurons.

Animals↗

PubMed1998

Functional mapping of human sensorimotor cortex with electrocorticographic spectral analysis. II. Event-related synchronization in the gamma band.

It has been shown in animals that neuronal activity in the 'gamma band' (>30 Hz) is associated with cortical activation and may play a role in multi-regional and multi-modal integration of cortical processing. Studies of gamma activity in human scalp EEG have typically focused on event-related synchronization (ERS) in the 40 Hz band. To assess further the gamma band ERS further, as an index of cortical activation and as a tool for human functional brain mapping, we recorded subdural electrocorticographic (ECoG) signals in five clinical subjects while they performed visual-motor decision tasks designed to activate the representations of different body parts in sensorimotor cortex. ECoG spectral analysis utilized a mixed-effects analysis of variance model in which within-trial temporal dependencies were accounted for. Taking an exploratory approach, we studied gamma ERS in 10-Hz-wide bands (overlapping by 5 Hz) ranging from 30 to 100 Hz, and compared these findings with changes in the alpha (8-13 Hz) and beta (15-25 Hz) bands. Gamma ERS (observed in three out of subjects) occurred in two broad bands-'low gamma' included the 35-45 and 40-50 Hz bands, and 'high gamma' the 75-85, 80-90, 85-95 and 90-100 Hz bands. The temporal and spatial characteristics of low and high gamma ERS were distinct, suggesting relatively independent neurophysiological mechanisms. Low gamma ERS often began after onset of the motor response and was sustained through much of it, in parallel with event-related desynchronization (ERD) in the alpha band. High gamma ERS often began during, or slightly before, the motor response and was transient, ending well before completion of the motor response. These temporal differences in low and high gamma suggest different functional associations with motor performance. Compared with alpha and beta ERD, the topographical patterns of low and high gamma ERS were more discrete and somatotopically specific and only occurred over contralateral sensorimotor cortex during unilateral limb movements (alpha and beta ERD were also observed ipsilaterally). Maps of sensorimotor function inferred from gamma ERS were consistent with maps generated by cortical electrical stimulation for clinical purposes. In addition, different task conditions in one subject produced consistent differences in both motor response latencies and onset latency of gamma ERS, particularly high gamma ERS. Compared with alpha and beta ERD, the topography of gamma ERS is more consistent with traditional maps of sensorimotor functional anatomy. In addition, gamma ERS may provide complementary information about cortical neurophysiology that is useful for mapping brain function in humans.

Adult↗

PubMed2003

Power grip disinhibits the ipsilateral sensorimotor cortex: a TMS and fMRI study.

Electrophysiological studies have shown that forceful activation of the hand muscles (power grip) is accompanied by an increased excitability of the ipsilateral corticospinal system. This increase in excitability may be due to spinal or cortical mechanisms. Here we show with fMRI that this phenomenon is at least in part mediated at a cortical level. We used TMS to show that the increased ipsilateral excitability during a forceful maneuver leads to enhanced stimulus-response curves. fMRI was used to compare the activation during a repetitive hand movement with or without an accompanying power grip on the opposite site. The power grip reduced movement-related activation in the ipsilateral sensorimotor cortex. Peak deactivation was located in the left postcentral gyrus extending into the adjacent precentral gyrus. This finding suggests that a forceful activation of the hand muscles disinhibits a distinct functional representation in the ipsilateral sensorimotor cortex. Consequently, the excitability of the corticospinal system increases and less neuronal excitatory activity is needed to perform a given task. The results may be important for a variety of studies as they suggest that fMRI may show decreased hemodynamic response under conditions in which other neurophysiological methods have shown increased functional activity.

Brain Mapping↗

PubMed1979

Pontine and non-pontine pathways mediating early mossy fiber responses from sensorimotor cortex to cerebellum in the cat.

Stimulation of the cat's sensorimotor cortex evokes a short-latency mossy fiber field potential (N2) in the pars intermedia of the cerebellum. The fraction of the response carried by each of the six cerebellar peduncles was determined by comparing the field potentials before and after electrolytic lesions of individual cerebellar peduncles. The response evoked from the contralateral cerebrum is 3.5 times as large as that evoked from ipsilateral cerebrum. The size of the N2 wave from contralateral cerebral cortex is reduced to about half of the original size after electrolytic lesion of either the brachium pontis (BP) or the restiform body (RB) ipsilateral to the recording site, while only a small reduction in the size of N2 is observed after lesions of contralateral BP and RB. This indicates that inputs responsible for the generation of the N2 wave from contralateral cerebral cortex enter the cerebellum primarily through ipsilateral BP and RB. In contrast, the N2 wave from ipsilateral cerebral cortex is reduced by approximately one quarter following lesions of any one of the four RB's and BP's. Fibers in the brachium conjunctivum do not contribute to these responses. Observation on the P2 field potential, representing postsynaptic firing of granule cells, suggest that the cerebro-ponto-cerebellar and cerebro-reticulo-cerebellar mossy fiber pathways converge onto granule cells. Furthermore, these two inputs must arrive within 3 ms of each other in order to activate the granule cells. In addition, it is shown that BP lesions reducing the mossy fiber input lead to an increase in the climbing fiber input.

Animals↗

PubMed1998

Relationship between dendritic pruning and behavioral recovery following sensorimotor cortex lesions.

A unilateral injury to the forelimb area of the sensorimotor cortex results in an increase in dendritic arborization in the contralateral homotopic cortex which is followed by a pruning back of these dendritic arbors. The increase in arborization is due to an increase in the use of the unimpaired forelimb for postural-motor support; whereas, the dendritic pruning is related, in time, to the return to more symmetrical limb use, but is not prevented by the maintenance of asymmetrical limb use. Dendritic pruning can be prevented by administering an NMDA receptor antagonist (such as MK801 or ethanol) during the pruning phase. This manipulation also coincides with the chronic reinstatement of behavioral deficits. The purpose of this study was to see whether removing the antagonism of the NMDA receptor results in the eventual return of dendritic pruning and behavioral recovery. Therefore, MK801 was administered to lesioned animals starting at post-lesion day 18. One group received MK801 injections until day 60 (Lesion + MK60) and another lesioned group received MK801 until day 30 after which the injections were changed to saline until day 60 (Lesion + MK30). Lesion + MK60 animals showed a prevention of dendritic pruning as well as a chronic reinstatement of forelimb deficits. Lesion + MK30 animals also showed a prevention of dendritic pruning, however, they showed behavioral recovery. These findings suggest that pruning of dendritic arbors may not be directly related to behavioral recovery.

Animals↗

PubMed1997

Suppression of spatial localization of a cutaneous stimulus following transcranial magnetic pulse stimulation of the sensorimotor cortex.

Transcranial magnetic pulse stimulation (TMS) over the region of the sensorimotor cortex impairs both perception and tactile localization of cutaneous stimuli delivered to the fingers of the contralateral hand. The region of the scalp over which TMS results in impaired cutaneous localization coincides with the region over which TMS suppresses simple perception. TMS has a more profound effect on tactile localization than on simple detection of cutaneous stimuli. TMS disrupts tactile localization for 400 ms after tactile perception has returned to normal.

Electric Stimulation↗

PubMed1988

Influence of anomalous rectifier activation on afterhyperpolarizations of neurons from cat sensorimotor cortex in vitro.

1. Large neurons from layer V of cat sensorimotor cortex (Betz cells) were studied to determine the influence of the anomalous rectifier current (IAR) on slow afterhyperpolarizations (AHPs). The neurons were examined using intracellular recording and single-microelectrode voltage clamp in an in vitro brain slice preparation. 2. A faster medium-duration AHP (mAHP) and slower AHP (sAHP) followed repetitive firing (22, 23). The amplitude of the mAHP often increased or remained constant during membrane potential hyperpolarization. The membrane potential trajectory resulting solely from IAR activation was similar to the mAHP. 3. Postrepetitive firing voltage clamp was used to measure directly slowly decaying K+ currents (IK) and IAR at different membrane potentials. IK exhibited both a fast and slow decay. The time constants of the fast decay of IK and IAR activation were similar. IAR increased with hyperpolarization or raised extracellular K+ concentration [( K+]o), whereas both the fast and slow components of IK reversed or nulled near -100 mV and behaved as pure K+ currents in response to raised [K+]o. 4. To determine the precise contribution of IK and IAR to the AHP waveform, theoretical AHPs were computed using a quantitative model based on voltage-clamp measurements. The calculated AHPs were qualitatively similar to measured AHPs. The amplitude of the mAHP showed little change with hyperpolarization because of the increasing dominance of IAR at more negative membrane potentials. The sAHP was little affected by IAR activation. 5. Several model parameters subject to biological variation among Betz cells were varied in the calculations to determine their importance in the AHP waveform. With IK parameters held constant, the amplitude and time course of the mAHP depended on resting potential, membrane time constant, the kinetics of the anomalous rectifier conductance (GAR), and the maximum value of GAR. IAR activation could result in a biphasic AHP even when the fast decay of IK was omitted from the calculations. 6. A wider variation of model parameters revealed behavior that may be relevant to other neurons. Certain values of membrane or IAR activation time constants resulted in a monophasic AHP even when the fast decay of IK was present. The decay of a biphasic AHP could reflect either the onset of IAR or the fast decay of IK, depending on the relative value of their time constants. Procedures are outlined to discriminate between these possibilities using current clamp methods.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1990

[The effect of serotonin on the neuronal reactions of the sensorimotor cortex evoked by tactile and conditional acoustic stimulation].

Responses of the sensorimotor cortex neurons to tactile and conditional sound stimuli have been investigated before and after serotonin and lysergoamide iontophoretic application. Three functional neuronal groups were distinguished according to their responses to unconditional and conditional stimuli. It was shown that serotonin application facilitated early and late impulse responses to tactile stimuli, facilitated and modulated impulse responses of many cortical neurons to conditional stimuli. Changes in responses to conditioning occurred during initial phase of the placing reaction and just after initiation of the conditional movement. Serotonin application promoted involving new neurons in response to sound. All these changes in the reactions developed with unsignificant background activity fluctuation. It is supposed that facilitation of neuronal responses caused by serotonin was linked with activation of excitatory receptors (S2). An increase of the background and evoked impulse activity following application of lysergoamide may depend on inhibitory serotonin receptors (S1B).

Acoustic Stimulation↗

PubMed1996

Use-dependent exaggeration of neuronal injury after unilateral sensorimotor cortex lesions.

Unilateral injury to the forelimb representation area of the sensorimotor cortex (FL-SMC) in adult rats causes over-reliance on the unimpaired forelimb for postural-motor movements, as well as overgrowth of layer V pyramidal cell dendrites in the homotopic cortex of the noninjured hemisphere. The overgrowth appears to be use-dependent because it can be prevented by restricting movements of the unimpaired forelimb. Additionally, restricting the unimpaired forelimb in animals with FL-SMC damage results in significantly greater behavioral dysfunction when examined 2 d after cast removal (compared to that after impaired-limb immobilization, or no limb immobilization). In the present study, the long-term behavioral and anatomical effects of limb immobilization were examined. Animals with FL-SMC lesions were fitted with casts immediately after the lesion that immobilized the impaired forelimb, the unimpaired forelimb, or neither forelimb for 15 d. Immobilization of the nonimpaired forelimb resulted in chronic prevention of dendritic growth and severe and chronic behavioral deficits. In addition, immobilization of the nonimpaired forelimb resulted in a dramatic exaggeration of the neuronal injury, presumably attributable to forced overuse of the impaired limb. Immobilization of the impaired forelimb resulted in no detectable neural changes and in only slightly increased and longer-lasting behavioral asymmetries (compared to nonimmobilized, lesioned animals), presumably attributable to mild disuse of the impaired limb. Immobilization of a single forelimb in nonlesioned rats resulted in no significant behavioral or anatomical changes. Together, these results suggest that although behavioral experience can enhance neural growth after brain injury, the region surrounding the injury may be vulnerable to behavioral pressure during the early postlesion period.

Animals↗

PubMed2006

Functional MR imaging of the human sensorimotor cortex after toe-to-finger transplantation.

BACKGROUND: A model of toe-to-finger transplantation has been used in studying peripheral nerve regeneration and central reorganization. It was found that recovery of sensory perception depends not only on peripheral reinnervation but also on central integrative mechanisms. OBJECTIVE: Our aim was to investigate functional changes of the brain and somatotopic representation of the transplanted toes after toe-to-finger transplantation. MATERIALS AND METHODS: Six patients who had toe-to-finger transplantation from 3 to 8 years earlier underwent motor and sensory functional MR imaging studies of transplanted toes and opposite corresponding normal fingers. The motor task was performed by repetitively tapping of the transplanted toe or finger against the thumb, whereas the sensory task was applied by tactilely stimulating the pulp of the transplanted toe or finger. RESULTS: The main activation areas from both types of stimulations were located in the expected location of the finger homunculus of the primary sensorimotor cortex. In addition, activated volumes from the transplanted toes were significantly greater than those from the opposite fingers (P = .017 for motor task and P = .005 for tactile sensory task, paired samples Student t test). CONCLUSIONS: Functional recruitment in the primary sensorimotor cortex seemed to have occurred following toe-to-finger transplantation. The transplanted toe was somatotopically represented in the hand area.

Adolescent↗

PubMed1994

Comparative effects of fluoxetine, amitriptyline and serotonin on functional motor recovery after sensorimotor cortex injury.

A recent investigation of the effects of the antidepressants desipramine and trazodone on behavioral recovery in brain-injured animals suggested that antidepressants, which act to increase noradrenergic activity in the brain, may facilitate the rate of recovery, whereas those that act to increase serotonergic (5-HT) activity may hinder recovery and reinstate deficits in recovered animals. The present study was designed to evaluate these findings further by assessing the effect of a single intraperitoneal injection of fluoxetine (a relatively pure 5-HT reuptake blocker), amitriptyline (a mixed 5-HT and noradrenergic reuptake blocker with alpha 1-adrenergic receptor blocking activity) or a single intraventricular infusion of 5-HT on recovery of beam-walking ability in animals with a unilateral sensorimotor cortex injury. None of the drugs significantly affected the rate of recovery. Although fluoxetine was ineffective in reinstating the motor deficit in recovered animals, amitriptyline reinstated the deficit in a dose-dependent fashion. Infusion of 5-HT resulted in an extremely transient reinstatement of the deficit, which was largely attributable to its short-term sedative properties. These results suggest that 5-HT may be less involved in functional recovery than previously thought. They also add further support to previous findings that indicate that drugs which act to antagonize alpha 1-adrenergic activity (e.g., phenoxybenzamine) may interfere with motor recovery after sensorimotor cortex injury. An appreciation of the potential impact of certain antidepressants on functional recovery in brain-injured patients appears warranted.

Amitriptyline↗