NeuroRehabilitation

In his seminal article, Physiogenesis and Psychogenesis in the ‘Post-Concussional Syndrome,’ Lishman (1988) proposed that neurobiological factors account for the development of the post-concussion syndrome and psychological factors become primarily responsible for maintaining it in the chronic phase. Over the 20 years that followed, researchers have advanced our understanding of the etiology of the post-concussion syndrome. Our review of this evidence suggests that neurobiological and psychological factors play a causal role in post-concussion symptoms from the outset, and thus, Lishman's causal model should be updated. If we can clinically identify individuals on a trajectory of poor recovery in the acute post-injury stage, then we can direct secondary prevention towards modifiable risk factors.

Functional neuroimaging technologies are increasingly being used to predict cognitive/behavioral outcomes after the initiation of clinical interventions such as resective surgery or cognitive rehabilitation. We provide a conceptual model and a case example to explain how the results from various neuroimaging techniques can be integrated to answer important questions about clinical recovery such as whether neural reorganization has occurred and, if so, the type of adaptive cognitive mechanism driving this reorganization. This proposed framework and its use in interpreting neuroimaging outcomes studies should help uncover the principles that govern neural reorganization, and be of use to any patient for whom the risk, or potential benefit, of brain-based interventions is unknown.

The corticospinal tract (CST) is the most important neural tract for motor function in the human brain. Therefore, clarification of CST injury would be an important topic in traumatic brain injury (TBI) rehabilitation. In this review, I reviewed diffusion tensor imaging (DTI) studies on CST injuries in terms of etiology and recovery in patients with TBI. Although DTI has several unique advantages for research on CST injury in TBI, only a dozen DTI studies on this topic have been reported: etiology of CST injury (9 studies), recovery of CST injury (3 studies). As for the etiology of CST injury in TBI, the previous studies have demonstrated the usefulness of DTI in diagnosis of CST injury in cases of diffuse axonal injury, transtentorial herniation, cerebral hemorrhage, and cortical contusion; moreover, according to the severity of TBI. The three studies on recovery of CST injury focused on recovery of a CST injured by diffuse axonal injury. In the future, we suggest an increase in the total number of DTI studies on this topic. In particular, research on recovery of CST injury should be encouraged. Moreover, studies of the various recovery mechanisms related to the CST are necessary.

Abulia is a disorder of the executive and frontal lobe function. It is characterised by severe psychomotor slowing that is not due to depressive illness or catatonic schizophrenia. Abulia is thought to be due to disruption of the meso-cortico-limbic dopaminergic system. Preliminary evidence suggests that patients with abulia may respond to treatment with dopaminergic drugs. We extend this evidence by reporting a significant and sustained functional improvement in a severely abulic patient after treatment with co-beneldopa (Madopar).

Many studies have reported that stroke patients can be accompanied by motor deficit of the unaffected extremities as well as the affected extremities. This suggests that neural control of motor function of unaffected extremities might be changed following stroke. However, very little is known about this topic. Using functional MRI (fMRI), we investigated changes in neural control of motor function of the unaffected hand in hemiparetic patients with cerebral infarct. Thirty-five hemiparetic stroke patients were recruited for this study. fMRI was performed at 1.5T during either affected or unaffected hand flexion-extension movements. We evaluated motor function of the affected upper extremity using the upper Motricity index (UMI) and the medical research council (MRC) scale for finger extensor. From fMRI, LI (laterality index) was calculated for assessment of relative activity in the ipsilateral versus the contralateral primary sensorimotor cortex. Positive correlation between LIs was observed during affected and unaffected hand movements (r = 0.670, p = 0.000). LI of unaffected hand movements was also correlated with the affected UMI (r = 0.408, p = 0.015) and MRC of the affected hand extensor (r = 0.362, p = 0.033). We demonstrated that the ipsilateral (affected) motor cortex was recruited by unaffected hand movements in proportion to poor motor function of the affected upper extremity.

The present paper shows the result of an open prospective study performed to evaluate the tolerance and efficacy of a program for neurological restoration (PRN) in stroke patients. The PRN is organized 4 weeks cycles – 39 hours per week – and applied by a team of physical, occupational, and speech therapists, physiatrists, psychologists, clinicians and nurses; directed by a neurologist. The first phase of treatment aims to increase the physical capacity and tolerance to exercise. The second phase trains specific abilities (balance, posture, gait and handling). Drugs were only used to modulate physical or mood disorders, spasticity, or pain. The study was performed in 80 stroke patients attended in our institution (2005–2007). Only patients with a confirmed diagnosis of stroke in the carotid territories, over 15 years old, and not least than 6 months post-ictal evolution were included. Tolerance to treatment was very good, with only 4 adverse events not related to treatment. The neurological condition was evaluated using the Scandinavian Stroke Scale (SSS), and the functional condition using the Barthel Index (BI). The results show significant improvements both in the neurological (113.45 ± 1.59%) and functional (130.11 ± 5.17%) condition after one treatment cycle, which improved further when therapy continued for a second cycle (233.71 ± 7.76% and 207.62 ± 27.16% respectively). Severity of the impairment was not a negative predictor of the outcome. Age correlated negatively with the initial condition, but does not prevent improvement. Sex, time of evolution, affected hemisphere or interactions among them did not influence the outcome. These results demonstrate that the PRN is well tolerated and effective promoting recovery even in chronic stroke patients.

The arcuate fasciculus (AF) is the neural tract that connects Wernicke's area and Broca's area. The main role of the AF is speech repetition; therefore, injury to the AF typically causes conduction aphasia. We report on a patient who showed excellent recovery of aphasia despite complete injury of the AF due to a cerebral infarct. A 54-year-old, right-handed male presented with aphasia and right hemiparesis. Brain MRI showed an infarct in the left centrum semiovale and corona radiata. Diffusion tensor tractography for the AF was reconstructed using DTI-studio software. The Korean-Western Aphasia Battery (K-WAB) was used for measurement of language function. On K-WAB at 1 week after onset, his aphasia type was compatible with global aphasia (aphasia quotient: 12‰, fluency: 5‰, comprehension: 24‰, repetition: 15‰, and naming: 31‰). The patient underwent rehabilitative therapy, including language therapy and medication, which is known to facilitate recovery from aphasia, for a period of 24 months. His aphasia had improved to a nearly normal state at 30 months after onset; aphasia quotient: 93‰ (fluency: 91‰, comprehension: 92‰, repetition: 85‰, and naming: 96‰). The left AF showed a complete disruption on 27-month diffusion tensor tractography. Findings from this study suggest the possibility that aphasia might show good recovery, even in cases of severe injury of the AF.

The specific neuromuscular mechanisms for compromised muscle strength with PD, and the improvement that occurs with medication, have not been clearly delineated. This study assessed knee extension and flexion strength of PD patients whilst on and off medication and examined the neural mechanisms responsible for any changes. Ten idiopathic PD patients were assessed whilst on and off medication (⩾ 12-h after drug withdrawal), ∼ 7 days apart. Isometric strength of the knee extensors and flexors was assessed, and the interpolated twitch technique used to measure activation of the knee extensors. Surface EMG was also used to measure neural drive to the agonists and antagonists. Without medication isometric strength of the knee extensors (7%) and flexors (11%) was impaired and the interpolated twitch technique revealed activation of the knee extensors was reduced (8%, P = 0.005). Maximum agonist amplitudes for nkee extension and flexion were unchanged off-medication (0.59 < P < 0.77). The agonist and antagonist EMG-force relationships, and the maximum antagonist EMG, were unaffected by medication withdrawal. The decrease in knee extension strength when PD patients were off medication was due to reduced activation of the agonist muscle, rather than any change in antagonist co-activation, and these changes were associated with reduced locomotory performance.