Post-Stroke Cognitive Impairment is Frequent After Infra-Tentorial Infarct.

BACKGROUND AND PURPOSE: Post-stroke cognitive impairment is a common and well-known consequence of supra-tentorial infarct, but its prevalence and severity after infra-tentorial infarct is unclear. We compared the frequencies and prognostic value of domain-specific cognitive deficits after supra-tentorial and infra-tentorial infarct. METHODS: In a consecutive cohort of patients with first-ever stroke (N = 244) admitted to Helsinki University Hospital, 37 patients had an infra-tentorial infarct. Patients were assessed with a comprehensive neuropsychological examination 3 months post-stroke covering 9 cognitive domains and functional disability was assessed at 15 months with the modified Rankin Scale. RESULTS: There were no statistically significant differences between the frequencies of cognitive deficits in patients with infra-tentorial vs supra-tentorial infarct. Altogether 73% of patients with infra-tentorial infarct and 82% of patients with supra-tentorial infarct had impairment in at least one cognitive domain. Further 42% of patients with infra-tentorial infarct and 47% of those with supra-tentorial infarct had deficits in 3 or more cognitive domains. In patients with infra-tentorial infarct, visuo-constructional deficits were significantly associated with functional disability at 15 months (OR 9.0, 95%CI 1.3-62.5, p = 0.027). In patients with supratentorial infarct, executive deficits (OR 2.9, 95%CI 1.5-5.8, p = 0.002) and visuo-constructional deficits (OR 2.9, 95%CI 1.5-5.7, p = 0.001) showed associations with functional disability at 15 months. CONCLUSION: Cognitive deficits are as common in patients with infra-tentorial infarct as in those with supra-tentorial infarct, and it is important to recognize them to meet the needs of rehabilitation.

Recovery of the 20 Hz Rebound to Tactile and Proprioceptive Stimulation after Stroke.

Sensorimotor integration is closely linked to changes in motor-cortical excitability, observable in the modulation of the 20 Hz rhythm. After somatosensory stimulation, the rhythm transiently increases as a rebound that reflects motor-cortex inhibition. Stroke-induced alterations in afferent input likely affect motor-cortex excitability and motor recovery. To study the role of somatosensory afferents in motor-cortex excitability after stroke, we employed magnetoencephalographic recordings (MEG) at 1-7 days, one month, and 12 months in 23 patients with stroke in the middle cerebral artery territory and 22 healthy controls. The modulation of the 20 Hz motor-cortical rhythm was evaluated to two different somatosensory stimuli, tactile stimulation, and passive movement of the index fingers. The rebound strengths to both stimuli were diminished in the acute phase compared to the controls and increased significantly during the first month after stroke. However, only the rebound amplitudes to tactile stimuli fully recovered within the follow-up period. The rebound strengths in the affected hemisphere to both stimuli correlated strongly with the clinical scores across the follow-up. The results show that changes in the 20 Hz rebound to both stimuli behave similarly and occur predominantly during the first month. The 20 Hz rebound is a potential marker for predicting motor recovery after stroke.

Strength of ~20-Hz Rebound and Motor Recovery After Stroke.

BACKGROUND: Stroke is a major cause of disability worldwide, and effective rehabilitation is crucial to regain skills for independent living. Recently, novel therapeutic approaches manipulating the excitatory-inhibitory balance of the motor cortex have been introduced to boost recovery after stroke. However, stroke-induced neurophysiological changes of the motor cortex may vary despite of similar clinical symptoms. Therefore, better understanding of excitability changes after stroke is essential when developing and targeting novel therapeutic approaches. OBJECTIVE AND METHODS: We identified recovery-related alterations in motor cortex excitability after stroke using magnetoencephalography. Dynamics (suppression and rebound) of the ~20-Hz motor cortex rhythm were monitored during passive movement of the index finger in 23 stroke patients with upper limb paresis at acute phase, 1 month, and 1 year after stroke. RESULTS: After stroke, the strength of the ~20-Hz rebound to stimulation of both impaired and healthy hand was decreased with respect to the controls in the affected (AH) and unaffected (UH) hemispheres, and increased during recovery. Importantly, the rebound strength was lower than that of the controls in the AH and UH also to healthy-hand stimulation despite of intact afferent input. In the AH, the rebound strength to impaired-hand stimulation correlated with hand motor recovery. CONCLUSIONS: Motor cortex excitability is increased bilaterally after stroke and decreases concomitantly with recovery. Motor cortex excitability changes are related to both alterations in local excitatory-inhibitory circuits and changes in afferent input. Fluent sensorimotor integration, which is closely coupled with excitability changes, seems to be a key factor for motor recovery.

Modulation of the ∽20-Hz motor-cortex rhythm to passive movement and tactile stimulation.

BACKGROUND: Integration of afferent somatosensory input with motor-cortex output is essential for accurate movements. Prior studies have shown that tactile input modulates motor-cortex excitability, which is reflected in the reactivity of the ∽ 20-Hz motor-cortex rhythm. ∽ 20-Hz rebound is connected to inhibition or deactivation of motor cortex whereas suppression has been associated with increased motor cortex activity. Although tactile sense carries important information for controlling voluntary actions, proprioception likely provides the most essential feedback for motor control. METHODS: To clarify how passive movement modulates motor-cortex excitability, we studied with magnetoencephalography (MEG) the amplitudes and peak latencies of suppression and rebound of the ∽ 20-Hz rhythm elicited by tactile stimulation and passive movement of right and left index fingers in 22 healthy volunteers. RESULTS: Passive movement elicited a stronger and more robust ∽ 20-Hz rebound than tactile stimulation. In contrast, the suppression amplitudes did not differ between the two stimulus types. CONCLUSION: Our findings suggest that suppression and rebound represent activity of two functionally distinct neuronal populations. The ∽ 20-Hz rebound to passive movement could be a suitable tool to study the functional state of the motor cortex both in healthy subjects and in patients with motor disorders.