scholarly journals Mapping the human corticoreticular pathway with multimodal delineation of the gigantocellular reticular nucleus and high-resolution diffusion tractography

2021 ◽  
Author(s):  
Pierce Boyne ◽  
Mark DiFrancesco ◽  
Oluwole O. Awosika ◽  
Brady Williamson ◽  
Jennifer Vannest

ABSTRACTThe corticoreticular pathway (CRP) is a major motor tract that provides volitional input to the reticular formation motor nuclei and may be an important mediator of motor recovery after central nervous system damage. However, its cortical origins, trajectory and laterality are incompletely understood in humans. This study aimed to map the human CRP and generate an average CRP template in standard MRI space. Following recently established guidelines, we manually delineated the primary reticular formation motor nucleus (gigantocellular reticular nucleus [GRN]) using several group-mean MRI contrasts from the Human Connectome Project (HCP). CRP tractography was then performed with HCP diffusion-weighted MRI data (N=1,065) by selecting diffusion streamlines that reached both the frontal cortex and GRN. Corticospinal tract (CST) tractography was also performed for comparison. Results suggest that the human CRP has widespread origins, which overlap with the CST across most of the motor cortex and include additional exclusive inputs from the medial and anterior prefrontal cortices. The estimated CRP projected through the anterior and posterior limbs of the internal capsule before partially decussating in the midbrain tegmentum and converging bilaterally on the pontomedullary reticular formation. Thus, the CRP trajectory appears to partially overlap the CST, while being more distributed and anteromedial to the CST in the cerebrum before moving posterior to the CST in the brainstem. These findings have important implications for neurophysiologic testing, cortical stimulation and movement recovery after brain lesions. We expect that our GRN and tract maps will also facilitate future CRP research.HIGHLIGHTSThe corticoreticular pathway (CRP) is a major tract with poorly known human anatomyWe mapped the human CRP with diffusion tractography led by postmortem & animal dataThe CRP appears to originate from most of the motor cortices and further anteriorThe estimated CRP had distributed and bilateral projections to the brainstemThese findings have important implications for motor recovery after brain lesions

1997 ◽  
Vol 273 (3) ◽  
pp. R896-R904 ◽  
Author(s):  
H. A. Baghdoyan

Microinjecting cholinomimetics into the pontine reticular formation produces a state that resembles natural rapid eye movement (REM) sleep. Evocation of this REM sleeplike states is anatomically site dependent within the pons and is mediated by muscarinic receptors. The cellular and molecular mechanisms underlying cholinergic REM sleep generation and muscarinic receptor subtype involvement remain to be specified. This study tested the hypothesis that muscarinic receptor subtypes are differentially distributed within the oral and caudal divisions of rat pontine reticular nucleus. In vitro receptor autoradiography was used to localize and quantify M1, M2, and M3 binding sites in the pontine reticular formation and in pontine brain stem regions known to regulate REM sleep. M1-M3 binding sites were present in some REM sleep-related nuclei, such as dorsal raphe and locus ceruleus. The pontine reticular formation was found to have a homogeneous distribution of M2 binding sites across its rostral to caudal extent, indicating that anatomic specificity of cholinergic REM sleep induction cannot be accounted for by a differential density of muscarinic receptors.


1988 ◽  
Vol 60 (6) ◽  
pp. 1967-1981 ◽  
Author(s):  
W. S. Ammons

1. Studies were done to characterize responses of spinal neurons backfired from the ventrolateral medulla to renal and somatic stimuli. Experiments were performed on 31 cats that were anesthetized with alpha-chloralose. Sixty-six spinal neurons were antidromically activated from the area of the lateral reticular nucleus or the ventrolateral reticular formation just rostral to the lateral reticular nucleus contralateral to the recording site. These cells could not be backfired from the medial reticular formation or from the spinothalamic tract just caudal to the thalamus. 2. Cells were located in laminae I, V, and VII of the T12-L2 segments. Antidromic conduction velocities averaged 35.9 +/- 7.2 m/s. Conduction velocities were unrelated to the projection site or laminar location of the cells. Termination sites of 21 cells were located in antidromic mapping experiments. Terminals were localized to the ventrolateral reticular formation, including the lateral reticular nucleus. 3. Responses to electrical stimulation of the renal nerves were always excitatory. Stimulation of renal A-delta-fibers excited 33 cells. These cells failed to respond to stimulation of renal C-fibers. The other 33 cells responded to both A-delta- and C-fiber stimulation. Latencies to A-delta-fiber stimulation averaged 9 +/- 2 ms, whereas latencies to C-fiber stimulation averaged 57 +/- 10 ms. 4. Renal mechanoreceptors were activated by occlusion of the renal vein or upper portion of the ureter. Renal vein occlusion excited 14 of 32 cells tested. Activity increased from 6 +/- 2 to 14 +/- 4 spike/s. Ureteral occlusion increased activity of 19 of 32 cells from 7 +/- 2 to 16 +/- 5 spikes/s. Cells responding to one of the mechanical stimuli were significantly more likely to receive A-delta-and C-fiber input compared with nonresponding cells. Nonresponders were more likely than responders to receive only A-delta input. 5. All cells received somatic input in addition to renal input. Twelve cells were classified as wide dynamic range, 46 as high threshold, and 8 as Deep. Somatic receptive fields most often included skin and muscle of the left flank and abdomen. Thirty-two cells had bilateral receptive fields, and 22 had inhibitory fields in addition to excitatory fields. 6. These data show that spinal neurons projecting to the ventrolateral medulla receive convergent inputs from the kidney and somatic structures. These cells may participate in a variety of functions including autonomic reflexes of renal origin.


1997 ◽  
Vol 77 (1) ◽  
pp. 435-451 ◽  
Author(s):  
Ewa Kostarczyk ◽  
Xijing Zhang ◽  
Glenn J. Giesler

Kostarczyk, Ewa, Xijing Zhang, and Glenn J. Giesler, Jr. Spinohypothalamic tract neurons in the cervical enlargement of rats: locations of antidromically identified ascending axons and their collateral branches in the contralateral brain. J. Neurophysiol. 77: 435–451, 1997. Antidromic activation was used to determine the locations of ascending spinohypothalamic tract (SHT) axons and their collateral projections within C1, medulla, pons, midbrain, and caudal thalamus. Sixty-four neurons in the cervical enlargement were antidromically activated initially by stimulation within the contralateral hypothalamus. All but one of the examined SHT neurons responded either preferentially or specifically to noxious mechanical stimuli. A total of 239 low-threshold points was classified as originating from 64 ascending (or parent) SHT axons. Within C1, 38 ascending SHT axons were antidromically activated. These were located primarily in the dorsal half of the lateral funiculus. Within the medulla, the 29 examined ascending SHT axons were located ventrolaterally, within or adjacent to the lateral reticular nucleus or nucleus ambiguus. Within the pons, the 25 examined ascending SHT axons were located primarily surrounding the facial nucleus and the superior olivary complex. Within the caudal midbrain, the 23 examined SHT ascending axons coursed dorsally in a position adjacent to the lateral lemniscus. Within the anterior midbrain, SHT axons traveled rostrally near the brachium of the inferior colliculus. Within the posterior thalamus, all 17 examined SHT axons coursed rostrally through the posterior nucleus of thalamus. A total of 114 low-threshold points was classified as collateral branch points. Sixteen collateral branches were seen in C1; these were located primarily in the deep dorsal horn. Forty-five collateral branches were located in the medulla. These were primarily in or near the medullary reticular nucleus, nucleus ambiguus, lateral reticular nucleus, parvocellular reticular nucleus, gigantocellular reticular nucleus, cuneate nucleus, and the nucleus of the solitary tract. Twenty-six collateral branches from SHT axons were located in the pons. These were in the pontine reticular nucleus caudalis, gigantocellular reticular nucleus, parvocellular reticular nucleus, and superior olivary complex. Twenty-three collateral branches were located in the midbrain. These were in or near the mesencephalic reticular nucleus, brachium of the inferior colliculus, cuneiform nucleus, superior colliculus, central gray, and substantia nigra. In the caudal thalamus, two branches were in the posterior thalamic nucleus and two were in the medial geniculate. These results indicate that SHT axons ascend toward the hypothalamus in a clearly circumscribed projection in the lateral brain stem and posterior thalamus. In addition, large numbers of collaterals from SHT axons appear to project to a variety of targets in C1, the medulla, pons, midbrain, and caudal thalamus. Through its widespread collateral projections, the SHT appears to be capable of providing nociceptive input to many areas that are involved in the production of multifaceted responses to noxious stimuli.


1983 ◽  
Vol 80 (3) ◽  
pp. 582-600 ◽  
Author(s):  
Nayef E. Saadé ◽  
Naman A. Salibi ◽  
Nabil R. Banna ◽  
Arnold L. Towe ◽  
Suhayl J. Jabbur

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Kyung Bo Lee ◽  
Joon Sung Kim ◽  
Bo Young Hong ◽  
Young Dong Kim ◽  
Byong Yong Hwang ◽  
...  

Although studies have demonstrated that several specific brain lesions are related to the severity of functional outcomes, the effects of specific brain lesions are not yet clear. This study investigated the effects of hemorrhagic stroke lesions on motor recovery. Eleven subjects with hemorrhagic stroke were assessed. Using the Fugl-Meyer Assessment and functional ambulation category, clinical motor and sensory impairments were tested four times in total: initially within 2 weeks and 1, 3, and 6 months after the onset of stroke. Brain lesions and size were evaluated using MRIcron, SPM8, and Talairach Daemon software. Trunk control, motor function in the lower limbs, and sensory function improved significantly within 3 months, after which the change was no longer significant. Upper limb function and gait were unchanged within 1 month but improved significantly 3 months after onset and continued to improve for 6 months. Involvement of the anterior putamen, internal capsule, thalamus, periventricular white matter, and premotor cortex was related to poor upper limb recovery in patients with hemorrhagic stroke. These results should be useful for planning rehabilitation strategies and understanding the prognosis of hemorrhagic stroke.


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