Arto C. Nirkko

Brain functional magnetic resonance imaging of rectal pain and activation of endogenous inhibitory mechanisms in irritable bowel syndrome patient subgroups and healthy controls

Background and aims: Many patients with irritable bowel syndrome (IBS) show intestinal hypersensitivity to distension and sensitisation after repeated intestinal distensions. Abnormalities in endogenous pain inhibitory mechanisms, such as diffuse noxious inhibitory controls (DNIC), may be implicated and were investigated during brain functional magnetic resonance imaging (fMRI). Patients and methods: fMRI was performed in 10 female patients with IBS (five constipated (IBS-C) and five with diarrhoea (IBS-D)) and 10 female healthy controls during rectal balloon distension alone or during activation of DNIC by painful heterotopic stimulation of the foot with ice water. Rectal pain was scored with and without heterotopic stimulation (0 = none, 10 = maximal). Results: Heterotopic stimulation decreased median rectal pain scores significantly in healthy controls (−1.5 (interquartile range −2 to −1); p = 0.001) but not in IBS-C (−0.7 (−1 to 0.5)), IBS-D (−0.5 (−1.5 to 0.5)), or in all IBS patients (0 (−1.5 to 1.3)). Brain activation changes during heterotopic stimulation differed highly significantly between IBS-C, IBS-D, and controls. The main centres affected were the amygdala, anterior cingulate cortex, hippocampus, insula, periaqueductal gray, and prefrontal cortex, which form part of the matrix controlling emotional, autonomic, and descending modulatory responses to pain. Conclusions: IBS-C and IBS-D appear to have differing abnormal endogenous pain inhibitory mechanisms, involving DNIC and other supraspinal modulatory pathways.

Different Ipsilateral Representations for Distal and Proximal Movements in the Sensorimotor Cortex: Activation and Deactivation Patterns

Each hemisphere is known to be also involved in controlling the ipsilateral arm, but with an asymmetry favoring the dominant hemisphere. However, the relative role of primary and secondary motor areas in ipsilateral control is not well defined. We used whole brain functional magnetic resonance imaging in healthy human subjects to differentiate between contributions from primary and secondary areas during discrete unilateral distal finger and proximal shoulder movements. It was found that ipsilateral distal movements activated secondary areas only, while sparing or even significantly deactivating the primary sensorimotor cortex. Ipsilateral proximal movements substantially activated both SM1 and secondary areas. A newly defined small territory within the precentral gyrus, extending from the premotor cortex and intruding toward SM1, showed an activation pattern corresponding to secondary motor areas. Finally, the effects of hemispheric dominance were confirmed, but attributed exclusively to secondary areas. These new imaging findings agree well with functional requirements as well as established anatomical and neurophysiological data.

Retardation of myelination due to dietary vitamin B12 deficiency: cranial MRI findings.

Vitamin B12 deficiency is known to be associated with signs of demyelination, usually in the spinal cord. Lack of vitamin B12 in the maternal diet during pregnancy has been shown to cause severe retardation of myelination in the nervous system. We report the case of a 14 1/2-month-old child of strictly vegetarian parents who presented with severe psychomotor retardation. This severely hypotonic child had anemia due to insufficient maternal intake of vitamin B12 with associated megaloblastic anemia. MRI of the brain revealed severe brain atrophy with signs of retarded myelination, the frontal and temporal lobes being most severely affected. It was concluded that this myelination retardation was due to insufficient intake of vitamin B12 and vitamin B12 therapy was instituted. The patient responded well with improvement of clinical and imaging abnormalities. We stress the importance of MRI in the diagnosis and follow-up of patients with suspected diseases of myelination.

Functional organisation of saccades and antisaccades in the frontal lobe in humans: a study with echo planar functional magnetic resonance imaging

The cortical activation pattern of saccades and antisaccades (versus rest) in the frontal lobe was analysed using an echo planar imaging (EPI) technique in 10 healthy subjects. Statistical analysis of activity in the dorsolateral prefrontal cortex disclosed a significantly greater activation during antisaccades in this region than during saccades. On the other hand, activity in the frontal eye fields was not statistically different in both tasks. These results confirm the important role of the dorsolateral prefrontal cortex for the correct performance of antisaccades obtained by studies in humans with isolated lesions of the dorsolateral prefrontal cortex.

Transient Cerebral Circulatory Arrest Coincides With Fainting in Cough Syncope

Article abstract-During prolonged coughing, intrathoracic and intra-abdominal pressures are transmitted via the great veins to the intracranial compartment, causing transient elevated intracranial pressure. The resulting reduction of cerebral perfusion pressure may cause a critical impairment of cerebral blood flow (CBF). Obstructive airway disease seems to be a prerequisite to build up the intrathoracic and intracranial pressures to a degree sufficient to compromise CBF and cause cough syncope. Using transcranial Doppler sonography (TCD) monitoring of middle cerebral artery flow velocities, we studied three patients with cough syncope. During coughing, they showed a transient cerebral circulatory arrest, which coincided with loss of consciousness in the two patients who fainted during TCD monitoring. EEG showed slowing, heart rate increased, and systemic arterial BP in one patient was preserved during the syncope. Our findings support the hypothesis that a critical reduction of CBF causes cough syncope. NEUROLOGY 1995;45: 498-501

Evolution of sleep and sleep EEG after hemispheric stroke

The evolution of subjective sleep and sleep electroencephalogram (EEG) after hemispheric stroke have been rarely studied and the relationship of sleep variables to stroke outcome is essentially unknown. We studied 27 patients with first hemispheric ischaemic stroke and no sleep apnoea in the acute (1–8 days), subacute (9–35 days), and chronic phase (5–24 months) after stroke. Clinical assessment included estimated sleep time per 24 h (EST) and Epworth sleepiness score (ESS) before stroke, as well as EST, ESS and clinical outcome after stroke. Sleep EEG data from stroke patients were compared with data from 11 hospitalized controls and published norms. Changes in EST (>2 h, 38% of patients) and ESS (>3 points, 26%) were frequent but correlated poorly with sleep EEG changes. In the chronic phase no significant differences in sleep EEG between controls and patients were found. High sleep efficiency and low wakefulness after sleep onset in the acute phase were associated with a good long‐term outcome. These two sleep EEG variables improved significantly from the acute to the subacute and chronic phase. In conclusion, hemispheric strokes can cause insomnia, hypersomnia or changes in sleep needs but only rarely persisting sleep EEG abnormalities. High sleep EEG continuity in the acute phase of stroke heralds a good clinical outcome.

Hypoxia-Induced Acute Mountain Sickness is Associated with Intracellular Cerebral Edema: A 3 T Magnetic Resonance Imaging Study

Acute mountain sickness is common among not acclimatized persons ascending to high altitude; the underlying mechanism is unknown, but may be related to cerebral edema. Nine healthy male students were studied before and after 6-h exposure to isobaric hypoxia. Subjects inhaled room air enriched with N2 to obtain arterial O2 saturation values of 75 to 80%. Acute mountain sickness was assessed with the environmental symptom questionnaire, and cerebral edema with 3 T magnetic resonance imaging in 18 regions of interest in the cerebral white matter. The main outcome measures were development of intra- and extracellular cerebral white matter edema assessed by visual inspection and quantitative analysis of apparent diffusion coefficients derived from diffusion-weighted imaging, and B0 signal intensities derived from T2-weighted imaging. Seven of nine subjects developed acute mountain sickness. Mean apparent diffusion coefficient increased 2.12% (baseline, 0.80±0.09; 6 h hypoxia, 0.81 ± 0.09; P = 0.034), and mean B0 signal intensity increased 4.56% (baseline, 432.1 ±98.2; 6 h hypoxia, 450.7 ± 102.5; P < 0.001). Visual inspection of magnetic resonance images failed to reveal cerebral edema. Cerebral acute mountain sickness scores showed a negative correlation with relative changes of apparent diffusion coefficients (r = 0.83, P = 0.006); there was no correlation with relative changes of B0 signal intensities. In conclusion, isobaric hypoxia is associated with mild extracellular (vasogenic) cerebral edema irrespective of the presence of acute mountain sickness in most subjects, and severe acute mountain sickness with additional mild intracellular (cytotoxic) cerebral edema.

Role of the corpus callosum in bimanual coordination: a comparison of patients with congenital and acquired callosal damage

The objective of the study was to investigate temporal control in patients with congenital as compared to acquired pathology of the corpus callosum during two different bimanual paradigms: (i) a drawer‐opening task during which one hand opened a drawer while the other hand reached and grasped a small object, and (ii) rhythmical circling movements that were executed according to the in‐phase or antiphase mode. Synchronization values revealed that patients with acquired callosal dysfunction generally showed optimal behaviour during the goal‐directed and familiar drawer‐opening task but demonstrated strong tendencies towards desynchronization during circling movements, which became most apparent for antiphase coordination. Whereas one patient with callosal agenesis showed a similar performance, the other acallosal patients performed both activities successfully. These observations indicate that patients with congenital absence of the corpus callosum can make use of compensatory mechanisms for allowing temporal synchronization during bimanual movements whereas patients with acquired callosal dysfunction are severely hampered when the task places significant demands on the control processes. The data also underline that the ability of callosal patients to precisely time events in coordinated actions depend on the task constraints.

Visual and Spectral Analysis of Sleep EEG in Acute Hemispheric Stroke

Background: Reports on the effects of focal hemispheric damage on sleep EEG are rare and contradictory. Patients and Methods: Twenty patients (mean age ± SD 53 ± 14 years) with a first acute hemispheric stroke and no sleep apnea were studied. Stroke severity [National Institute of Health Stroke Scale (NIHSS)], volume (diffusion-weighted brain MRI), and short-term outcome (Rankin score) were assessed. Within the first 8 days after stroke onset, 1–3 sleep EEG recordings per patient were performed. Sleep scoring and spectral analysis were based on the central derivation of the healthy hemisphere. Data were compared with those of 10 age-matched and gender-matched hospitalized controls with no brain damage and no sleep apnea. Results: Stroke patients had higher amounts of wakefulness after sleep onset (112 ± 53 min vs. 60 ± 38 min, p < 0.05) and a lower sleep efficiency (76 ± 10% vs. 86 ± 8%, p < 0.05) than controls. Time spent in slow-wave sleep (SWS) and rapid eye movement (REM) sleep and total sleep time were lower in stroke patients, but differences were not significant. A positive correlation was found between the amount of SWS and stroke volume (r = 0.79). The slow-wave activity (SWA) ratio NREM sleep/wakefulness was lower in patients than in controls (p < 0.05), and correlated with NIHSS (r = –0.47). Conclusion: Acute hemispheric stroke is accompanied by alterations of sleep EEG over the healthy hemisphere that correlate with stroke volume and outcome. The increased SWA during wakefulness and SWS over the healthy hemisphere contralaterally to large strokes may reflect neuronal hypometabolism induced transhemispherically (diaschisis).

Human cortical plasticity Functional recovery with mirror movements

Cortical plasticity of the human brain permits functional recovery after brain injury even in the absence of neuronal recovery. We report the combined evaluation, including electrophysiology and functional magnetic resonance imaging, of the pattern of cortical and cerebellar reorganization, in a patient with mirror movements as a sequel of perinatal unilateral brain injury. Recovery resulted in motor control by the healthy hemisphere using direct ipsilateral corticospinal projections and the contralateral cerebellum.