Long-term recovery from a minimally responsive state with recovery of an injured ascending reticular activating system: A case report.

ABSTRACT: We report on a patient with hypoxic-ischemic brain injury (HI-BI) who showed recovery from a minimally consciousness state over 6 years concurrent with recovery of an injured ascending reticular activating system (ARAS), which was demonstrated on diffusion tensor tractography (DTT).A 31-year-old female patient, who suffered from HI-BI, showed impaired consciousness with a minimally conscious state: intermittently obeying simple motor tasks, such as "please grasp my hand." Her consciousness showed recovery with the passage of time; rapid recovery was observed during the recent 2 years.In the upper ARAS, the neural connectivity to both the basal forebrain and prefrontal cortex had increased on 8-year DTT compared with 1.5-year DTT. In the lower dorsal and ventral ARAS, no significant change was observed between 1.5 and 8 years DTTs.Recovery of an injured ARAS was demonstrated in a patient who showed recovery from a minimally consciousness state over 6 years following HI-BI. Our results suggest the brain target areas for recovery of impaired awareness in patients with disorders of consciousness.

Difference between injuries of the corticospinal tract and corticoreticulospinal tract in patients with diffuse axonal injury: a diffusion tensor tractography study.

Objectives: No studies have investigated differences in injury of the corticospinal tract (CST) and corticoreticulospinal tract (CRT) following diffuse axonal injury (DAI) to date. Therefore, we investigated differences in injury of the CST and CRT in patients with DAI using diffusion tensor tractography (DTT).Methods: Twenty consecutive patients with DAI and 20 control subjects were recruited. CST and CRT were reconstructed. Each part of the CST and CRT was analyzed in terms of DTT parameters and configuration.Results: Upon group analysis, decreased FA and TV values were observed in both the CST and CRT in the patient group compared with the control group (%) (p < .05). In the individual analysis in terms of the TV, significantly higher injury incidence was observed for the CRT (47.5%) than the CST (25.0%) (p < .05). Evaluation of the DTT configuration revealed significantly higher injury incidence for the CRT (50.0%) than the CST (17.5%) (p < .05). Specifically, the incidence of discontinuation was significantly higher for the CRT (40.0%) than the CST (10.0%) (p < .05).Conclusions: Injury of the CST and CRT was detected in patients with DAI using DTT. In terms of the incidence and severity of neural injury, the CRT appeared to be more vulnerable to DAI than the CST.

Recovery of Hypersomnia Concurrent With Recovery of an Injured Ascending Reticular Activating System in a Stroke Patient: A Case Report.

We report on a stroke patient who showed recovery of hypersomnia concurrent with the recovery of an injured ascending reticular activating system (ARAS), which was demonstrated by diffusion tensor tractography (DTT).A 70-year-old female patient underwent coiling of the left ruptured posterior communicating artery after subarachnoid hemorrhage and both extraventricular drainage for management of an intraventricular hemorrhage. At 2 months after onset, when she started rehabilitation, she exhibited intact consciousness, with the full score on the Glasgow Coma Scale: 15. However, she showed severe hypersomnia: she always fell asleep without external stimulation and the Epworth Sleepiness Scale (EPS) score was 24 (full score: 24, cut off for hypersomnia: 10). She underwent comprehensive rehabilitative therapy, including neurotropic drugs, physical therapy, and occupational therapy. Her hypersomnia has shown improvement as 14 (3 months after onset), 11 (4 months after onset), 7 (12 months after onset), and 6 (24 months after onset), respectively.On 2-month DTT, narrowing of both lower dorsal and ventral ARASs was observed on both sides: in particular, among 4 neural tracts of the lower ARAS, the right lower ventral ARAS was the narrowest. By contrast, on 24-month DTT, the 4 narrowed neural tracts of both lower dorsal and ventral ARASs were thickened compared with those of 2-month DTT.Recovery of hypersomnia with recovery of an injured lower ARAS on DTT was observed in a stroke patient. Our results suggest that evaluation of the lower ARAS using DTT might be useful for stroke patients with hypersomnia.

Recovery of injured lower portion of the ascending reticular activating system in a patient with traumatic brain injury.

The authors report on a patient with traumatic brain injury who showed recovery of an injured lower portion of the ascending reticular activating system (ARAS) between the pontine reticular formation and the thalamus. A 57-yr-old male patient experienced head trauma. After 4 mos from onset, he exhibited impaired alertness, with a score of 7 on the Glasgow Coma Scale. At 40 mos after onset, the patient had a full Glasgow Coma Scale score of 15. The lower portion of the ARAS was reconstructed using the probabilistic tractography method. On 4-mo diffusion tensor tractography, the fractional anisotropy and the tract volume of the lower portion of the right ARAS were lower by more than 2 SDs of those of control subjects. By contrast, on 40-mo diffusion tensor tractography, the fractional anisotropy and the tract volume values of the lower portion of the right ARAS were within 2 SDs of those of the control subjects. The increment fractional anisotropy and the FV value of the lower portion of the right ARAS on 40-mo diffusion tensor tractography indicated recovery of the injured lower ARAS. As a result, recovery of an injured lower portion of the ARAS in a patient with traumatic brain injury was demonstrated.

Recovery of an injured corticoreticular pathway via transcallosal fibers in a patient with intracerebral hemorrhage.

BACKGROUND: Several studies have reported on injury of the corticoreticular pathway (CRP), however, little is known about the mechanism for recovery of an injured CRP. We report on a patient with intracerebral hemorrhage (ICH) who showed recovery of an injured CRP via transcallosal fibers, which was demonstrated by diffusion tensor tractography (DTT). CASE PRESENTATION: A 67-year-old man presented with complete paralysis (Medical Research Council: 0/5) of the left extremities at the onset of a right putaminal hemorrhage. At six weeks after onset, he presented with more severe weakness of proximal joint muscles than distal joint muscles (right shoulder abductor; 2-, finger extensor; 3+, hip flexor; 2+, ankle dorsiflexor; 3). Although his right hemiplegia had recovered well, he consistently showed more severe proximal weakness (right shoulder abductor; 3, finger extensor; 4, hip flexor; 3+, ankle dorsiflexor; 4) until 16 weeks after onset. On both six- and 16-week DTTs, in the left (affected) hemisphere, the CRP showed severe narrowing with discontinuation of the anterior fibers at the corona radiata on six-week DTT, however, the discontinued anterior fibers of the CRP were connected to the right cerebral cortex via transcallosal fibers on 16-week DTT. CONCLUSION: We demonstrated recovery of an injured CRP via transcallosal fibers in a patient with ICH. We believe that this might be a mechanism for recovery of an injured CRP.

Injury of the corticoreticular pathway in patients with proximal weakness following cerebral infarct: diffusion tensor tractography study.

The corticoreticular pathway (CRP) innervates mainly the proximal muscles of extremities. Identification of the CRP by diffusion tensor tractography (DTT) in the human brain has recently become possible. However, little is known about the relation between proximal weakness and injury of the CRP in stroke patients. In this study, we attempted to investigate the usefulness of DTT for elucidation of the relation between proximal motor weakness and injury of the CRP in patients with cerebral infarct. Among 247 consecutive patients with cerebral infarct, four hemiparetic patients who showed more severe weakness in proximal joints (shoulder and hip) than distal joints (finger and ankle) of the affected extremities were recruited for this study. Evaluation of motor function, DTT, and transcranial magnetic stimulation (TMS) for evaluation of the corticospinal tract state by analysis of the characteristics of the motor-evoked potential were performed at the early stage of cerebral infarct (mean: 17.0 days; range: 11-29). The integrity of the CST on DTT findings in the affected hemisphere was preserved in all four patients and TMS findings in terms of latency and amplitude showed within normal range (one patient) and partial injuries (three patients) of the corticospinal tract. By contrast, on DTT of the CRP in the affected hemispheres, we observed Wallerian degeneration in two patients and discontinuations at infarct level in two patients. The injury of the CRP appeared to attribute the proximal weakness of the shoulder and hip observed in these four patients. Therefore, DTT of the CRP would be useful for elucidating the relation between proximal weakness and injury of the CRP in patients with cerebral infarct.

Head and eye movements in rats with pontine reticular lesions in comparison with primates: a scientific memoir and a fresh look at some old and 'new' data.

The author recounts the process of discovery in Philip Teitelbaum's laboratory, which began with the observation of vestibular head stabilization in a rat with brainstem lesions, of the essential roles of the pontine reticular formation (PRF) in the rat in ipsiversive head as well as eye movements. The PRF in the rat appears to be in the pathways for most direction-changing movements of the eyes and head, leaving vestibular and optokinetic stabilizing movements intact and uninterrupted. The author postulates that a response to the sliding of feet or paws, or a "substrate-kinetic reflex," works together with vestibular and optokinetic reactions to stabilize an animal's directions of gaze and locomotion on the ground. Previously unpublished data are presented from later observations and recordings of rats with kainic acid lesions in the PRF, which support the conclusion that neurons in the PRF are essential for head as well as eye movements in the rat. In contrast, Volker Henn observed no obvious loss of head movements in monkeys that had a loss of fast eye movements from kainic acid lesions of the PRF. The author and others observed that quick phases of head nystagmus develop some time after quick phases of ocular nystagmus in normal human infants; in other words, after the PRF is functioning for eye movements. The author concludes that in primates, the pathway for head movements through the PRF has been replaced by a newer pathway, leaving certain PRF regions to be devoted to mediating only eye movements.

Increased GABAergic activity in the region of the pedunculopontine and deep mesencephalic reticular nuclei reduces REM sleep and impairs learning in rats.

Newly formed memories are initially fragile and require consolidation to be transformed into an enduring state. Memory consolidation may occur during increased postlearning REM sleep. REM deprivation during these periods (termed REM sleep windows [RSWs]) impairs subsequent performance. The pedunculopontine nucleus (PPT) and adjacent deep mesencephalic reticular nuclei (DpMe) have been implicated in the generation of REM sleep. Following 24-hr baseline recording, rats were trained on the 2-way avoidance task for 50 trials/day over 2 days and retested on Day 3. EEG was recorded 22 hr after training on training Days 1 and 2. Rats were injected with the GABAB agonist baclofen or saline into the PPT/DpMe region at 0300 to coincide with the start of a known RSW. Based on shuttle performance, saline rats were assigned post hoc to a learning group (LG) that avoided the footshock at least 60% at retest or nonlearning group (NLG) that performed below this criterion. Baclofen-injected rats were not assigned post hoc into separate groups as all rats performed below the learning criterion. PPN/DpMe infusions of the inhibitory GABAB agonist baclofen decreased REM and impaired subsequent memory performance. Normal GABAergic transmission in the PPN/DpMe may be necessary for REM to occur and for the consolidation of incentive learning.

Neonatal-onset brainstem reticular reflex myoclonus following a prenatal brain insult: generalized myoclonic jerk and a brainstem lesion.

Brainstem reticular reflex myoclonus (BRRM) is characterized by sudden, generalized, shock-like movements that can be elicited by sensory stimulation. We present a boy, born after 35 weeks gestation, who was diagnosed with neonatal-onset BRRM. Within 1 hr of birth, the patient showed spasticity and generalized clonic movements of all limbs elicited with tactile stimulation anywhere on the body. Surface electromyography showed co-contraction of agonistic and antagonistic muscles, revealing that his generalized clonic movements were tremulous myoclonus in nature. Brain magnetic resonance imaging (MRI) at 21 hrs after birth disclosed high-intensity lesions in the Rolandic area, thalamus, basal ganglia, and brainstem, including the dorsal pons and medulla, the center of BRRM, in T1-weighted images. Follow-up MRI at 1 month revealed dramatic improvement in the pontine lesion. The patient showed gradual remission of the characteristic movements, which disappeared at 1 year of age, but the patient died unexpectedly at 1 year and 3 months. In conclusion, neonatal BRRM arises as a result of severe brainstem injury, and the associated lesions may only be seen temporarily on MRI taken soon after birth.

Changes occur in the ability to promote axonal regeneration as the post-injury period increases.

This study tested whether adult rat brain stem neurons could respond to growth or trophic factors provided after an extended post-injury period. The number of neurons that regenerated their axon into a peripheral nerve graft following exposure to ciliary neurotrophic factor (CNTF) 8 weeks after a cervical lesion was comparable to the number regenerating after exposure to CNTF 4 weeks after injury. In contrast, there was a significant decrease of 50% in the number of regenerating neurons following exposure to basic fibroblast growth factor (bFGF) 8 weeks after injury compared with the number regenerating after treatment with bFGF 4 weeks after injury. These results indicate that some factors are effective promoters of regeneration only if provided within a defined post-injury period.

Plasticity of fin command system function following spinal transection in larval sea lamprey.

The descending control of dorsal fin posture by a reidentifiable reticulospinal command neuron (I1), was examined in the sea lamprey, Petromyzon marinus. Intracellular stimulation of I1 controls the posture of both dorsal fins. Spinal transection between the fins results not only in loss of control of posterior dorsal fin posture, but after 2 h, the control of the anterior dorsal fin as well. Anterior dorsal fin responses remained absent at 4, 5 and 6 days after transection. Stimulation of I1 could control anterior dorsal fin posture in specimens which had recovered the ability to right during swimming (77 and 100 days after transection), although higher than normal stimulus frequencies were required. I1 control of posterior dorsal fin posture did not recover.

Generalized epilepsy evoked by freeze lesions in the mesencephalon of the cat.

Epilepsy was induced by making freeze lesions bilaterally in the mesencephalic reticular formation of cats. The convulsive activity was an equivalent of the generalized status epilepticus, devaloping 15-20 min after the freeze lesions had been made. The animals died in this state 16-20 h after it had developed. The generalized seizure activity may have spread to rostra1 structures from the lesioned mesencephalic reticular formation generalizing instantenously, or have been triggered and maintained by a local irritative zone, surrounding the necrotized tissue caused by freezing. The cooling of the same cryoprobes, by which the freeze lesions had been made, had no effect on the status epilepticus, probably because only the necrotized tissue was cooled. The cooling of the inferior thalamic peduncles changed the pattern of epileptic discharges, indicating that thalamocortical structures played a role in sustaining it.

Pontine gaze paresis due to traumatic craniocervical hyperextension. Report of two cases.

Pontine gaze paresis is frequently due to tumor of the brain stem. Occasionally it may be caused by inflammation or ischemia. Two cases are reported, each with pontine gaze paresis and other signs of lower brain-stem injury, basal skull fractures, and second cervical vertebra fractures. This pattern of injuries is believed to be the result of craniocervical hyperextension with stretch injury to the brain stem at the junction of the medulla and pons.