[Incidence and clinico-anatomical characteristics of severe vascular accidents of the brain stem].
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The given study aimed to answer the question about the realization in clinical practice of the possibility of the timely identification of the degree of intracranial hypertension in patients with cerebral stroke under continuous monitoring of the intracranial volume/pressure ratios by means of examination of CSF changes and CT of the head. On the basis of an analysis of the interrelationship between the severity of neurologic deficit, findings of CT of the head and the results of examination of the cerebral hemodynamics the authors evaluated the informativeness of the main parameters of monitoring the intracranial volume/pressure ratios in the acute stage of cerebral stroke. It has been found that only prolonged registration of the mean and pulse pressure of the CSF in combination with "testing the reserve of the intracranial volume" may ensure the timely detection of disorders of the homeostasis of the craniospinal reservoir and the selection of the most effective means of their correction.
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Short latency somatosensory evoked potentials (S-SEP) to median nerve stimulation recorded from scalp-shoulder derivation consisted of four positivities (P1, P2, P3 and P4) and one negativity (N). There is still, however, significant controversy regarding the generators of these peaks. The purpose of the present study is to attempt to solve some of the controversies by comparing the potentials recorded on surface montages with intrasurgical tracing obtained while monitering evoked potentials. This is complemented by analysis of S-SEP in patients with disorders of the cervical cord, brain stem or thalamus. Average latency of each component in normal subjects (N = 17) was as follows; P1: 7.6 +/- 0.6 ms P2: 9.6 +/- 0.7 ms, P3: 11.8 +/- 0.8 ms, P4: 12.9 +/- 0.5 ms, N: 17.7 +/- 0.8 ms. The peak latency of P1 was always shorter than that of negativity recorded over the Erb's point following the median nerve stimulation. The peak latency of P2 corresponded to that of the earliest negativity of spinal evoked potential, recorded from the epidural dorsal surface of the lower cervical cord during the operation, which was considered as the potential of afferent volley at the posterior root or spinal entry portion. In a case with severe spondylotic radiculopathy, P2 and following components were abolished. The peak latency of P3 corresponded to that of negative potential recorded over the high cervical dorsal column or cuneate nucleus.(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke is the most common neurologic disorder of adults and one of the three leading causes of death in North America. Results of a study suggest that inexpensive and easily obtained clinical variables can be used to predict which patients with stroke will do well and which will not. This capability is invaluable to physicians, patients with stroke and their families, and future investigators.
Hypersomnia is described in 11 patients who have had a cerebral circulation episode with prevalent localization of the lesion in the oral divisions of the brain trunk. Three morphological observations are presented: these were cases of bilateral affection of certain meso- and diencephalic structures, e.g. medial divisions of the thalami and the diencephalon cover with involvement of the grey matter of the Sylvian aqueduct into the process. The observations presented confirm the opinion that the nonspecific structures of the meso- and diencephalic region are a part of the complex cortico-subcortical system participating in maintaining the state of wakefulness.
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The clinical findings were compared with the results of morphological examination of the brain in 32 patients who had died in different periods after surgery for removal of neurinoma of the acoustic nerve. In all cases vessels supplying the brain stem were injured during removal of the tumor. In 5 cases all three groups of arteries of the pons varolii were injured, which led to the development of infarction of half of the pons. The short circumflex pons arteries and the anterior inferior cerebellar artery were injured in 18 patients, which caused the formation of an infarct in the lateral part of pons varolii. The distal segment of the anterior inferior cerebellar artery was injured in 9 patients, as a result of which a small focus of infarction formed in the dorsolateral parts of the pons.
Consciousness can be studied only if subjective experience is documented and quantified, yet first-person accounts of the effects of brain injury on conscious experience are as rare as they are potentially useful. This report documents the alterations in waking, sleeping, and dreaming caused by a lateral medullary infarct. Total insomnia and the initial suppression of dreaming was followed by the gradual recovery of both functions. A visual hallucinosis during waking that was associated with the initial period of sleep and dream suppression is described in detail. Since the changes in sleep and their recovery are comparable to results of animal experiments, it can be concluded that damage to the medullary brain stem causes extreme but short-lived alterations in conscious state and that substantial recovery occurs even though the damage to the brain stem endures.
Torpid facial ulcerations may occur as a result of lesions involving the trigeminal fibers. These neurotrophic ulcerations have usually been observed after alcohol injection in the trigeminal ganglion. We report two cases associated with brainstem infarction. In both patients, the blink reflex was studied. The masseter inhibitory reflex was studied in one case. Analysis of these electrophysiological recordings can be of particular value in localizing the site of the lesion along the trigeminal pathway.
OBJECTIVE: to evaluate clinical, radiological, and prognostic features of patients with multiple acute infarcts in remote arterial territories of the posterior circulation. DESIGN: Data analysis from a prospective acute stroke registry in a community based primary care centre using a standard protocol including MRI and MRA. RESULTS: In three and a half years, 27 of the 236 patients (11%) with posterior circulation stroke had multiple acute infarcts in the posterior circulation as shown by gadolinium enhancement on MRI. Eighteen patients had multiple infratentorial and supratentorial infarcts including the cerebellum and posterior cerebral artery territory, with coexisting brainstem involvement in seven patients. Fourteen patients had a rostral basilar artery syndrome and cerebellar signs; four patients had a visual field defect with cerebellar signs. Causes were vertebral (six) or basilar (four) artery atheromatosis, and cardioembolism (four). Seven patients had multiple acute infarcts in the posterior circulation of the cerebellum and lower brainstem. Brainstem and cerebellar signs were found in most patients (five); aetiologies were small vessel disease (four), cardioembolism (one), and vertebral artery dissection (one). Two patients with large artery atheromatosis had multiple acute infarcts in the posterior circulation in the brainstem and posterior cerebral artery territory. One month after stroke more than 25% of the patients were dependent or had died. There was no difference in the outcome between the three groups, and recovery was linked to the size of infarcts rather than to a high number of infarcts. CONCLUSIONS: multiple acute infarcts in the posterior circulation usually involve the cerebellum. Simultaneous brainstem and posterior cerebral artery territory infarcts sparing the cerebellum are uncommon. They can be suspected clinically before neuroimaging, mainly when supratentorial and infratentorial infarcts coexist. This may be important, because different patterns of infarction are associated with different causes of stroke.
One hundred and six elderly patients with chronic stroke who were admitted to Seiai Rehabilitation Hospital were studied regarding urinary incontinence. The average age of the subjects was 74 +/- 8 years old, ranging from 60 to 94 years. Seventy three of the 106 patients (69%) had urinary incontinence which was found in 72% of brain infarction, 61% of brain hemorrhage and 67% of subarachnoid hemorrhage. The prevalence of urinary incontinence in cases of brain stem, thalamic, and putaminal hemorrhage was 80%, 67% and 46%, while that in cases of cortical infarction and infarct of perforating arteries was 84% and 68%, respectively. The rate of urinary incontinence was significantly higher in those aged 75 years or over (p < 0.05), those with poor activities of daily living (ADL, p < 0.005), or with dementia (p < 0.001). Dementia was a complicating factor more frequently in aged patients (p < 0.05) and in those with poor ADL (p < 0.001), although no correlation was seen between age and ADL (p = 0.08). These results indicated the high prevalence of urinary incontinence in elderly inpatients with chronic stroke, which is significantly related to impairment of mental and physical activities.
Nine patients with brainstem infarct and two with brainstem haemorrhage presented with pure motor stroke, pure supranuclear facial palsy, sensorimotor stroke or ataxic hemiparesis. Despite the clinical similarity with hemispheric lacunes, brainstem infarcts causing lacunar syndromes probably have a greater tendency to progress. Small brainstem haemorrhages should also be considered as a cause of lacunar syndromes and the difficulty in differentiating them from small infarcts without CT is emphasised.
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Middle cerebral artery occlusion (MCAO) is a widely used surgical procedure for inducing focal cortical ischaemia in mice. In the present study, all experiments were performed on 4-week-old, male Swiss mice (OF-1 Iffa Credo, France), 20-25 g at the time of surgery. Sham-operated mice were subjected to simple exposure of the middle cerebral artery. Mice were injected with either MK-801, ifenprodil, JO 1784, JO 1994 or JO 1997 at the following time points after surgery; 5, 15, 45 min and 3, 6, 24, 30, 48 and 54 h. Mice were sacrificed 72 h after surgery and both ipsilateral and contralateral cortices were dissected in their entirety, weighed, and assayed for [3H]PK 11195 binding while the brain-stem and cerebellum were assayed for nitric oxide synthase (NO synthase) activity. In a separate experiment the area of ischaemic damage was determined planimetrically by means of an image analysis system. Coagulation of the middle cerebral artery induced a marked enhancement of the ipsilateral cortical omega 3 peripheral-type benzodiazepine binding site (PTBB'S) densities, an increase in NO synthase activity in the brain-stem and cerebellum, and an increase in the cortical infarct area. MK-801, ifenprodil, JO 1784, JO 1994 and JO 1997 demonstrated comparable neuroprotective effects on all three indices of cortical damage. A down-regulation of cortical omega 3 peripheral-type benzodiazepine binding site (PTBB'S) densities and a decrease in NOS activity occurred following pharmacological intervention. In contrast to JO 1784, JO 1994 and JO 1997 have a bimodal effect on omega 3 PTBB'S densities.
Multiinfarct dementia is the second most common form of dementia in the elderly. An animal model of microischemia may provide information about the pathophysiology relevant when searching for prevention or treatment of microinfarctions in humans. The purpose of the present study was to develop an experimental model useful for studying discrete microischemic foci. In order to achieve single cerebral microischemic foci plastic beads with diameters of about 100 microns were injected into the left heart ventricle of anesthetized rabbits. 2-Deoxy-[14C]glucose (2-DG) and autoradiography were used to detect regions with disturbed metabolism. The tissue sections were inspected for impacted beads. Foci with markedly increased 2-DG accumulation and with diameters of about 1 mm were detected in all parts of the brain, indicating hypoxic regions with enhanced glycolysis. In some foci, located mainly in the basal ganglia, a central dip in the 2-DG profile was seen, suggesting poor glucose supply to the central ischemic region. The ratio foci/beads was about 1 in the brain stem (diencephalon included) and about 0.5 in the cortex. Twenty-four hours after embolization, infarctions, mainly in the deeper brain regions, were seen. There were still foci with increased 2-DG uptake, which were mainly located in the cortex. The results suggest that microemboli reaching the deeper brain regions give rise to metabolic disturbances more often than emboli reaching the cortex and that the ischemic foci in deeper brain regions are more prone to develop further into infarctions.