CORRELATION INDICES OF CEREBRAL HEMODYNAMICS AND ELECTRICAL ACTIVITY IN CHILDREN WITH IMPAIRED MOTOR SKILLS.

The correlations between the indicators of cerebral hemodynamics and electrical activity in children with impaired motor skills of central origin (children with cerebral palsy) were investigated. There is established a high number of links between indicators of rheoencephalogram (REG) and electroencephalogram (EEG) in the left cerebral hemisphere than in the right. In frontomastoidal allocation 19 correlations and in occipitomastoidal - 59 links. We suppose that poor circulation in vertebroplasty-basilar system leads to the defeat of the brain stem, which, with afferent pathways of the reticular formation, connects the thalamus with the cortex. In the reticular formation there is an inhibition of ascending activators influences, which eland to decreasing of the cortex is tonus. You can talk about the functional immaturity of the system of nonspecific activation by the reticular formation of the brain stem. Children with violation of motor activity had significantly more negative and positive significant and high correlation among the existing indicators of electric brain activity and cerebral hemodynamics, in our opinion, is due to the development of interconnection compensation that is carried out by adjustment of the functional systems and the formation of new forms of adaptive responses in conditions of disontogenetik. Feature correlation pattern of the EEG, of children with disorders of motor activity, is associated with a significantly great number of high and significant correlations between measures of electrical brain activity in the δ- and q- rhythms, especially in the temporal areas of the cerebral cortex. According to visual analysis of EEG there is revealed a common manifestation of changes of bioelectric brain activity in children with disorders of motor activity. This is manifested in the development of paroxysmal activity of action potentials of θ- and δ-rhythms with the focus of activity in the anterior areas of the cerebral cortex; the formation of a mosaic representation of the θ-rhythms in temporal areas; the presence of hypersynchronous a-paroxysms in the posterior areas of the cerebral cortex. The given facts testify to activation of mechanisms of limbic-neocortical systems and synchronizing influences of the reticular formation of the stem and diencephalic structures. There is also detected greater number of correlations when occipitomastoidal registration was lone it reflects compensatory redistribution of cerebral blood flow over the affected structures of brain stem structures that are associated with the provision of cortical functions.

Temporary reduction of blood pressure and sympathetic nerve activity in hypertensive patients after microvascular decompression.

BACKGROUND AND PURPOSE: Experimental studies suggested neurovascular compression of the brain stem as a cause of hypertension. The aim of our prospective study was to investigate the effect of microvascular decompression in patients with severe hypertension with neurovascular compression on blood pressure and central sympathetic nerve activity in the long-term. METHODS: Fourteen patients (4 males; mean age, 46+/-8 years) with essential hypertension underwent microvascular decompression of the brain stem. Vasoconstrictor muscle sympathetic nerve activity (recorded by microneurography: burst frequency, bursts/min) and blood pressure (24-hour profiles) were investigated before surgery and 7 days, 3 months, and every 6 months postoperatively. RESULTS: Muscle sympathetic nerve activity was preoperatively elevated and decreased significantly postoperatively (35+/-13 bursts/min vs 20+/-9 bursts/min; P<0.01). Sympathetic activity remained reduced 3 months (19+/-8 bursts/min; P<0.01), 6 months (19+/-7 bursts/min; P<0.01), and 12 months (23+/-9 bursts/min; P<0.01) postoperatively. However, in the long-term, sympathetic nerve activity increased again (18 months after surgery: 28+/-10 bursts, not significant; 24 months postoperatively: 34+/-12 bursts/min, not significant). Systolic and diastolic blood pressure decreased from 162+/-6/98+/-5 mm Hg preoperatively to 133+/-6/85+/-4 mm Hg (7 days postoperatively; P<0.01); 136+/-5/86+/-4 mm Hg (3 months postoperatively; P<0.01); 132+/-4/85+/-4 mm Hg (6 months postoperatively; P<0.01); 132+/-3/85+/-5 mm Hg (12 months postoperatively; P<0.01); 132+/-5/84+/-5 mm Hg; P<0.01). Twenty-four months after microvascular decompression, blood pressure increased again up to 158+/-7/96+/-6 mm Hg, corresponding to the sympathetic nerve activity course. CONCLUSIONS: Sympathetic nerve activity and blood pressure are temporary reduced by microvascular decompression in patients with severe hypertension with neurovascular compression. The data are a hint for sympathetic overactivity as a pathomechanism in this subgroup of patients.

Neurons in the preBötzinger complex and VRG are located in proximity to arterioles in newborn mice.

The constant cyclic respiratory activity in the brainstem requires an un-interrupted blood flow providing glucose and O(2) to neurons generating respiratory rhythm. Here we used a combination of classical vascular visualization techniques, and calcium imaging, to compare the microvascular structure and localization of active respiratory neurons in the brainstem of newborn mice at the level of the preBötzinger complex (PBC) and ventral respiratory group. The brainstem is supplied with perforating arteries, which enter primarily in the midline and in a circumscribed region mid-laterally in the medulla. Presumed arterioles then pass dorso-medially with a high density immediately lateral to the midline, and mid-laterally at approximately 60% of the midline-to-lateral edge distance. Calcium imaging, using Fluo-8, AM, showed that active PBC/VRG neurons are located in the same region where a high density of arterioles is found. We conclude that the striking co-localization of medullary arterioles and the PBC/VRG could imply that respiratory neurons may derive part of their glucose and oxygen consumption directly from arterioles, and that humoral factors affecting ventilation may reach respiratory neurons by precapillary transport mechanisms.

Medullary microvessel degeneration in multiple system atrophy.

Multiple system atrophy (MSA) is a rare and fatal early-onset autonomic disorder which is characterised by Parkinsonism and orthostatic hypotension (OH). The pathophysiology of MSA is not fully understood but key features include the depletion of medullary autonomic neurons and presence of glial cellular inclusions. We hypothesise that the degeneration of medullary autonomic microvessels is an additional finding in MSA. Using digital pathology we quantified basement membrane collagen (Coll IV), smooth muscle actin (alpha-actin) and endothelial glucose transporter (Glut 1) expression in medullary autonomic nuclei of 8 MSA and 8 OH cases, compared with 12 controls with no autonomic dysfunction. We found decreased Coll IV (p=0.000) and Glut 1 (p=0.000) but not alpha-actin expression, in medullary autonomic nuclei of MSA, but not OH cases compared with control subjects. Medullary microvessel degeneration in MSA may be secondary to the primary neuro-glial pathogenesis of the disorder, and could accelerate its ageing-related progression.

Activity of midbrain reticular formation and neocortex during the progression of human non-rapid eye movement sleep.

To clarify the neural correlates and brain activity during the progression of human non-rapid eye movement (NREM) sleep, we examined the absolute regional cerebral blood flow (rCBF) during light and deep NREM sleep and during wakefulness in normal humans using positron emission tomography with H(2)(15)O. Relative changes in rCBF during light and deep NREM sleep in comparison to the rCBF during wakefulness were also analyzed. During light NREM sleep, the rCBF in the midbrain, in contrast to that in the pons and thalamic nuclei, did not decrease when compared to that during wakefulness, whereas rCBF decreased in the left medial frontal gyrus, left inferior frontal gyrus, and left inferior parietal gyrus of the neocortex. During deep NREM sleep, the rCBF in the midbrain tegmentum decreased, and there was a marked and bilateral decrease in the rCBF in all neocortical regions except for the perirolandic areas and the occipital lobe. There have been three groups of brain structures, each representing one type of deactivation during the progression of NREM sleep. The activity of the midbrain reticular formation is maintained during light NREM sleep and therefore represents a key distinguishing characteristic between light and deep NREM sleep. Selective deactivation of heteromodal association cortices, including those related to language, occurs with increasingly deep NREM sleep, which supports the recent theory that sleep is not a global, but it is a local process of the brain.

[Sudden loss of consciousness: clinical presentation and pathophysiologic mechanisms]. / Der plötzliche Bewusstseinsverlust: klinische Präsentation und pathophysiologische Mechanismen.

Most cases of sudden and temporary loss of consciousness [syncope] are caused by hypoperfusion of the formatio reticularis. more rarely by primary neurologic or metabolic disorders. The most common etiology is vasodepressor (vasovagal) syncope, which is caused by peripheral vasodilation due to acute withdrawal of the efferent sympathetic tone, while the parasympathetic outpour is increased at the same time. Although the efferent limb of the baroreflex manifests in a rather uniform way, the afferent parasympathetic limb is very variable, leading to a variety of clinical presentations and triggers (orthostatic hypotension, pain, fear, cough, micturition, emotions). While vasodepressor syncope mainly occurs in young people with healthy hearts, cardiac syncope caused by arrhythmias or obstructive lesions are more frequently found in elderly patients with organic heart disease. Neurogenic syncope comprises either primary neurologic disorders, such as epilepsia, or hypoperfusion of the vertebrobasilar system (TIA). Rarely, an acute increase of intracerebral pressure may cause syncope. Similarly, metabolic disorders or side effects of drugs are rare causes of syncope; however, drugs may act as important cofactors in the pathogenesis of syncope.

Activation by attention of the human reticular formation and thalamic intralaminar nuclei.

It has been known for over 45 years that electrical stimulation of the midbrain reticular formation and of the thalamic intralaminar nuclei of the brain alerts animals. However, lesions of these sectors fail to impair arousal and vigilance in some cases, making the role of the ascending activating reticular system controversial. Here, a positron emission tomographic study showed activation of the midbrain reticular formation and of thalamic intralaminar nuclei when human participants went from a relaxed awake state to an attention-demanding reaction-time task. These results confirm the role of these areas of the brain and brainstem in arousal and vigilance.

Essential hypertension: could the basic defect be in blood supply of vasomotor centre?

Various factors have been implicated in the pathogenesis of essential hypertension, although the exact cause of essential hypertension is still unknown. In this paper it is suggested that the basic pathology in essential hypertension may be an inherited defect in the blood supply of that part of reticular formation of rostral ventrolateral medulla which contains the pressor area. The posited defect is one in which the arterial branch supplying blood to the above-mentioned pressor area of vasomotor center arises from an artery which is stenosed. The other branches of this stenosed artery supply adjacent areas of medullary reticular formation concerned with other neurological functions. Due to this stenosis there is ischaemia of the pressor area resulting in increased systemic arterial pressure. During stress, the blood requirement of adjacent areas of the reticular formation (whose function is still not clearly defined) may increase, thus further decreasing blood flow to vasopressor area and increasing the cerebral ischaemic response. After a prolonged time, this increased blood pressure can cause hyaline arteriolar nephrosclerosis in kidney, which may participate in the maintenance of elevated systemic arterial pressure.

Remote cortical dysfunction as a possible cause of subcortical neglect? A regional cerebral blood flow study.

Cortical remote effects of right deep-seated lesions were studied with two cerebral blood flow measurement methods (two-dimensional xenon-133 inhalation and 99mTc HMPAO SPECT) in a population of 13 right-handed stroke patients. A neuropsychological battery of tests suitable for assessment of possible visual neglect was performed. Neglect was present in 7 cases. A regional cortical hypoperfusion was observed in all patients. However, in neglect patients it was more extended and involved the right inferior parietal region suggesting a causal relationship between cortical dysfunction and neuropsychological deficit. This finding supports the model attributing neglect to a unilateral attention-arousal defect in a cortico-limbic-reticular loop.

[Effect of ischemia on the gigantocellular nucleus in rats]. / Wplyw ischemii na ultrastrukture jadra olbrzymiokomórkowego u szczura.

The gigantocellular region of the reticular formation of the brain stem of rat was studied two weeks and one month after complete, 5-min ischemia. Edematous changes affected some large neurons, especially their dendrites, as well as some astrocytes. An increased number of polymorphic lysosomes and lipid droplets was observed in large neurons. Some of them exhibited an abundance of cytoskeleton elements, i.e., neurotubules and neurofilaments. These ultrastructural changes persisted one month after the ischemic incident.

Selective saccadic palsy caused by pontine lesions: clinical, physiological, and pathological correlations.

Two patients suffered a selective deficit of voluntary saccades and quick phases of nystagmus after hypoxic-ischemic insults during open-heart surgery. All voluntary saccades, in both horizontal and vertical planes, were slow, and quick phases of vestibular and optokinetic nystagmus were absent. Smooth pursuit, the vestibuloocular reflex, the ability to hold steady eccentric gaze, and vergence eye movements were all preserved. Pathological studies in 1 patient confirmed neuronal necrosis and gliosis, consistent with ischemic lesions involving the median and paramedian pontine reticular formation and median basis pontis but sparing the rostral mesencephalon and rostral interstitial nucleus of the medial longitudinal fasciculus. These findings, taken with data from experimental studies, support the hypothesis that each functionally defined class of horizontal eye movements is controlled by a separate neural substrate that projects independently to the abducens nuclei. In addition, these data suggest that the rostral interstitial nucleus of the medial longitudinal fasciculus is dependent on inputs from the paramedian pontine reticular formation for the programming of normal vertical saccades.

Unilateral left paramedian infarction of thalamus and midbrain: a clinico-pathological study.

In a patient with a unilateral embolic infarct in the left posterior thalamo-subthalamic paramedian artery territory, neuropathological studies showed involvement of the intralaminar, dorsomedial, and internal part of the ventral posterior nuclei of the thalamus, of the rostral part of the mesencephalic reticular formation, and of the posterior commissure. The patient showed upgaze palsy for voluntary saccades, smooth pursuit and vestibulo-ocular movements, sustained downgaze, right-sided motor hemineglect and facio-brachial hypaesthesia, motor transcortical aphasia and anterograde amnesia. This case confirms that unilateral destruction of the posterior commissure, rostral interstitial nucleus of the MLF and interstitial nucleus of Cajal produces a non-dissociated upgaze palsy. Involvement of the nucleus of Cajal probably produced the sustained downward deviation of the eye, by causing predominance of downward vestibulo-ocular inputs. This case also shows that thalamic aphasia and anterograde amnesia may be related to a paramedian lesion of the thalamus, with special reference to involvement of the dorsomedial nucleus, in the absence of lesion of the pulvinar and mamillo-thalamic tract and of conspicuous involvement of the ventral lateral nucleus. Selective hemineglect for motor tasks may occur in infarction of the dominant thalamus, involving the intralaminar nuclei.

One-and-a-half syndrome in ischaemic locked-in state: a clinico-pathological study.

Five patients with "locked-in" syndrome and dysconjugate palsy of horizontal gaze were studied. In all cases internuclear ophthalmoplegia due to dysfunction or destruction of the median longitudinal fasciculus was combined with an ipsilateral gaze palsy, producing the "one-and-a-half" syndrome. Clinical and electro-oculographic examination suggested involvement of the paramedian pontine reticular formation when all ipsilateral saccades were abolished, when exotropia of the contralateral eye was present, and when vestibular stimulation showed full conjugate deviation to the damaged side. Involvement of the abducens nucleus was suggested when the palsy of ipsilateral gaze was not dissociated on vestibular stimulation. In three cases these clinical deductions were confirmed by the pathological study, which showed a corresponding destruction of the median longitudinal fasciculus, paramedian pontine reticular formation and abducens nucleus. In one case the one-and-a-half syndrome evolved into a total horizontal gaze palsy, which corresponded to involvement of the abducens nucleus contralateral to the initially destroyed paramedian pontine reticular formation. Vertical oculocephalic response disappeared, because of destruction of the median longitudinal fasciculus on both sides (bilateral internuclear ophthalmoplegia). Patients with the locked-in syndrome provide a unique situation in which complex pontine oculomotor disturbances may be studied, because consciousness is preserved. In these patients, dissociated and dysconjugate oculomotor palsy may have been underestimated.

[Functional state of the hippocampo-reticular complex during submaximal physical loading and fatigue]. / Funktsional'noe sostoianie gippokampo-retikuliliarnogo kompleksa pri submaksimal'noi fizicheskoi nagruzke i utomlenii.

On 22 rabbits with bipolar electrodes chronically implanted in the dorsal hippocampus and the mid-brain reticular formation, it has been established that a submaximal physical load in non-trained animals results in a stable drop of excitability of the studied structures. In the process of a 30-day training programme the hippocampus excitability was lowered, while the reticular formation excitability after a short-term lowering increased and returned to the initial level on the 20th day of training. On the EEG of the studied structures, high-amplitude activity predominated, local blood flow increased only in the reticular formation. The nature of functional interrelations of the studied structures changed both in the non-trained animals and during training.

Transient global amnesia--a hippocampal phenomenon?

A case of transient global amnesia of clear vascular aetiology is described. Results of neuropsychological testing carried out during the attack clarify the nature of the memory disorder and suggest that the critical region of ischaemia is the medial temporal area around the hippocampus. Follow-up testing suggests that no lasting memory impairment resulted.

[Effect of glycerin on several indices of intracranial hemodynamics and the electroencephalogram of wakeful cats with experimental intracerebral hemorrhage]. / Vliianie glitserina na nekotorye pokazateli vnutricherepnoi gemodinamiki i élektroéntsefalogrammu bodrstvuiushchikh kosehek s éksperimental'nym vnutrimozgovym krovoizliianiem.

An intravenous infusion of glycerin to cats 24-48 hours after an intracerebral hemorrhage contributes to normalization of the EEG, Intensifies the local blood flow in the visual cortex, thalamus and reticular formation of the midbrain in both hemispheres (predominantly in the regions of the right affected hemisphere). The drug produces a fall in the absolute values of the intracranial pressure without its secondary rise after infusion is discontinued and causes a moderate rise of the perfusion pressure. The intravenous infusion of glycerin is more effective than its single injection.