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Results for “Brain Stem Infarctions”

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PubMed1980

Computed tomography in brainstem hemorrhage.

Seven of eight patients had a clinical diagnosis other than brainstem hemorrhage before computed tomography (CT). Four were diagnosed as infarction, one as intracerebral hemmorrhage, one as hypertensive encephalopathy, and one as subdural hematoma. All survived except one, who died of pulmonary embolus. Although the yeild of posterior fossa lesions on CT is thought to be small, our experience indicates that CT is exceedingly valuable in demonstrating and localizing brainstem hemorrhage. The prognosis of brainstem hemorrhage appears to be better than reported in the literature.

Aged↗
PubMed1991

Doppler CO2-test in patients with vertebrobasilar ischemia.

The pathogenesis of vertebrobasilar ischemia (VBI) is still uncertain. Embolism and systemic hypotension have been discussed as possible causes. We evaluated the basilar arteries of 35 VBI-patients by transcranial Doppler-sonography at rest and under hypercapnic conditions and compared these findings with the basilar flow velocities in 10 healthy volunteers matched by age. We found no difference between the controls and the VBI-patients for the basilar flow velocities at rest. Under hypercapnia (end-tidal CO2-concentration 8.5%), the basilar blood flow velocities in the healthy controls increased by an average of 53.0% but only by 32.3% in the VBI-patients (p less than 0.005). The reduction of CO2 dependent vasomotor reactivity was observed in all VBI-patients, except in patients with infarction in the posterior cerebral artery area, possibly indicating a different pathogenic mechanism of stroke. The results in all other patients revealed no obvious correlation to the clinical course or angiographic or dopplersonographic findings. As CO2 dependent vasomotor reactivity and brain perfusion pressure dependent cerebral autoregulation have similar mechanisms, we conclude that systemic hypotension might play an important part in VBI.

Aged↗
PubMedDate not supplied

MRI in acute hemiplegia of childhood.

OBJECTIVE: Acute hemiplegia in childhood is rare, the underlying etiology frequently obscured and the pathological site unidentified. MATERIALS AND METHODS: Magnetic resonance imaging (1.5 T Magnetom) was performed in two cases with hemiplegia followed by repeated studies at 3 and 16 months, respectively, after the initial examinations, including CT and angiography, were negative. RESULTS: MRI demonstrated otherwise occult lesions in the brain stem and showed the subsequent partial resolution consistent with infarction. CONCLUSION: MRI should be employed in those children with acute hemiplegia in whom no underlying cause is elicited.

Acute Disease↗
PubMed1994

Vestibular syndromes in the roll plane: topographic diagnosis from brainstem to cortex.

Central vestibular syndromes may be classified according to the three major planes of action of the vestibuloocular reflex, secondary to a lesional tone imbalance in either the horizontal yaw plane or the vertical pitch or roll plane. The clinical signs, both perceptual and motor, of a vestibular tone imbalance in the roll plane are ocular tilt reaction (OTR), ocular torsion, skew deviation and tilts of the perceived visual vertical (SVV). Either complete OTR or skew torsion without head tilt indicates a unilateral peripheral deficit of otolith input or a unilateral lesion of graviceptive brainstem pathways from the vestibular nuclei (crossing midline at the pontine level) to the interstitial nucleus of Cajal (INC) in the rostral midbrain. SVV tilts are the most sensitive sign of a vestibular tone imbalance in roll and occur with peripheral or central vestibular lesions from the labyrinth to the vestibular cortex. All tilt effects, perceptual, ocular motor and postural, are ipsiversive (ipsilateral eye undermost) with unilateral peripheral or pontomedullary lesions below the crossing of the graviceptive pathways. All tilt effects are contraversive (contralateral eye undermost) with unilateral pontomesencephalic brainstem lesions and indicate involvement of the medial longitudinal fasciculus or the rostral midbrain (INC). Unilateral lesions of vestibular structures rostral to the INC typically manifest with deviations of perceived vertical without concurrent eye-head tilt. OTR in unilateral paramedian thalamic infarctions indicates simultaneous ischemia of the paramedian rostral midbrain including the INC. Unilateral lesions of the posterolateral thalamus can cause thalamic astasia and moderate ipsiversive or contraversive SVV tilts, thereby indicating involvement of the vestibular thalamic subnuclei. Unilateral lesions of the parietoinsular vestibular cortex cause moderate, mostly contraversive SVV tilts. An SVV tilt found with monocular but not with binocular viewing is typical for a trochlear or oculomotor palsy rather than a supranuclear graviceptive brainstem lesion.

Brain↗
PubMed1981

Dementia, deep white matter damage and hypertension: 'Binswanger's disease'.

The clinical and neuropathological features are reported of 7 patients with organic intellectual impairment or dementia, hypertension and ischaemic destruction predominantly of the deep white matter of the cerebral hemispheres resembling that seen in infarction. The white matter changes have been dismissed as rare n the past, usually under the name of Binswanger's disease or subcortical arteriosclerotic encephalopathy, and without much concern for hypertension. There are now indications that this sort of case may not be uncommon. It can be suspected in life on CT scans. The accuracy of assessment of the pathological substrate of organic dementia, and therefore the strategies of research and treatment, might well benefit from further clinicopathological studies.

Aged↗
PubMed1993

[Convergence-retraction nystagmus associated with vascular disorders of the brainstem].

We report two cases of convergence-retraction nystagmus due to cerebral infarction and hemorrhage. Magnetic resonance imaging disclosed a small area of abnormal signal in the thalamo-mesencephalic junction in each patient. This lesion appeared to include the rostral interstitial nucleus of the medial longitudinal fasciculus (rostral iMLF). The precise oculography of nystagmus in these patients demonstrated the fast adductive movements and slow exponential tract of abduction. The velocity of the fast phase was equal to or less than that of ordinary saccadic eye movements. The time constant of the slow phase was about 0.3 second. These characteristics are identical to those of pineal tumor cases.

Adolescent↗
PubMed1999

[Cerebral infarction accompanied by dysgeusia--a clinical study on the gustatory pathway in the CNS].

Dysgeusia was investigated in 11 patients with thalamic infarction and 13 patients with corona radiata infarction to locate the gustatory pathways based on the sites of the lesions. Dysgeusia was present in 4 out of 11 patients with thalamic infarction and 3 out of 13 patients with corona radiata infarction. The dysgeusia was contralateral to the lesion in all these patients. Cheiro-oral syndrome was observed as a complication in 2 patients each from both groups. The responsible lesion was located on the medial side of the ventral posterolateral (VPL) nucleus and the ventral posteromedial (VPM) nucleus in the patients with thalamic infarction who developed dysgeusia, and was located posteriorly to the corona radiata in the other group. In the patients without gustatory disturbance, on the other hand, the lesions showed no such spread. These findings suggest that the gustatory pathway ascends contralaterally in the cerebral hemisphere and that the pathway from the thalamus projects to the cerebral cortex via the posterior part of the corona radiata. It is also suggested that the pathways in the thalamus and corona radiata are very close to the sensory fibers from the mouth and hands projecting to the sensory area.

Aged↗
PubMed1995

Brain-stem auditory evoked potential monitoring. Variations of stimulus artifact in brain death.

Brain-stem auditory evoked potentials (BAEPs) were recorded in 20 subjects with brain death (mean age, 33.2 +/- 15.1 years) and 20 healthy volunteers (mean age, 29.8 +/- 6.8 years). Brain death was due to head injury (n = 14), encephalitis (n = 3), brain-stem hemorrhage (n = 1), cerebellar hemorrhage (n = 1) or cerebral infarction (n = 1). The presence, latency and amplitude of the individual BAEP components and variations of the stimulus artifact were evaluated. The mean (+/- S.D.) amplitude of the stimulus artifact was 0.26 +/- 0.12 microV in the brain-dead subjects and 0.09 +/- 0.05 microV in the control group (P < 0.001, t test). The causes of the phenomenon of increasing stimulus artifacts in the evolution of brain death remain unclear.

Acoustic Stimulation↗
PubMed1999

Analysis of the corneal reflex with air puff: normal controls and patient groups.

Though there are several reports published about the corneal reflex elicited by different methods, a standardized electrophysiologic study with air puff in man has not been published. The aim of this study is to standardize the corneal reflex elicited by air puff to cornea. The authors studied the corneal reflex with air puff and direct touch by using a standardized method in patients with thalamic hemorrhage (n = 15), hemispheric infarction (n = 9), brainstem infarction (n = 9), multiple sclerosis (n = 12), and Bell's palsy (n = 12) and in normal control subjects (n = 21). The conventional blink reflex (BR) was also studied. The reflex responses were recorded from both orbicularis oculi muscles by air puff and direct touch to cornea in addition to the electrical stimulation of the supraorbital nerve. No statistical difference could be detected between the responses elicited by air puff or direct touch to cornea (P > 0.05). Corneal reflex responses were statistically different from the R2 response of the BR (P < 0.005). Because the responses elicited by direct touch and air puff to cornea are identical, air puff to cornea can be used confidently to study the corneal reflex.

Adult↗
PubMed1992

Attenuation of dipoles modelled from SEP due to a lacunar infarct or altered stimulus rate.

In normal subjects and patients with sensory, sensorimotor or motor deficit, due to a unilateral infarct affecting the thalamocortical radiation, SEPs to median nerve stimulation were analyzed by a spatiotemporal dipole model which describes an evoked potential by a limited number of stationary dipoles with time varying amplitudes. In the normal subjects the SEPs were explained by one dipole in the brainstem and two dipoles in the cortical hand area contralateral to stimulation, all with different time courses. Increasing the stimulus rate to 6.2 Hz yielded a reduction of the moment of both cortical dipoles but hardly affected brainstem dipole moment. In the five patients with sensory or sensorimotor deficit the strength of one or both cortical dipoles was reduced on the side of the lesion. In the patients with pure motor deficit cortical dipole activity was normal. The brainstem dipole was preserved in all patients.

Adolescent↗
PubMedDate not supplied

Early, evolving Wallerian degeneration of the pyramidal tract in cerebrovascular diseases: MR study.

OBJECTIVE: The purpose of this study was to demonstrate the early features of the Wallerian degenerative process and their relationship with the severity of motor deficit. MATERIALS AND METHODS: Fourteen patients with infarction or hemorrhage of the basal ganglia were studied by MRI of the same coronal slice along the pyramidal line. RESULTS: The earliest sign of abnormal signal intensity was detected 0.7 month after the initial insult. On proton-density (PD) imaging, low signal intensity was observed on 11 (73.3%) of 15 occasions from 0.7 to 2.0 months, and abnormal signal intensity was not detected 5 (83.3%) of 6 times from 2.1 to 3.7 months. High signal intensity was revealed on 11 (78.6%) of 14 occasions after 3.8 months. The widest extent of the low-intensity signal band on PD imaging was closely related to the severity of motor deficits at > 4 months. CONCLUSION: The development of the Wallerian degenerative process was divided into four stages by MRI. We conclude that the extent of Wallerian degeneration is related to the severity of motor deficit.

Adult↗
PubMed1990

[Crossed cerebellar diaschisis after brainstem infarction].

Metabolic depression in the cerebellar hemisphere contralateral to supratentorial stroke termed "Crossed Cerebellar Diaschisis" (CCD) was first described by Baron and coworkers and now interpreted as a transneuronal deactivation resulted from loss of excitatory afferent inputs. Among the cerebrocerebellar pathways possibly involved, the corticopontocerebellar pathway is considered to be the most important to induce CCD. According to the hypothesis that CCD results from the destruction of the corticopontocerebellar pathway, any lesion wherever located in the corticopontocerebellar pathway may induce CCD. Little is known, however, about CCD after the brainstem lesion. Our case presented here showed that a brainstem lesion actually induced CCD and that CCD resulted from transneuronal deactivation. An 80-year-old female was admitted to the neurological department of Kasugai City Hospital because of left-sided hemiparesis of sudden onset on March 19, 1989. On admission and 5 days after admission CT scan of the brain was performed, but no stroke lesion was found. Magnetic resonance imaging of the brain disclosed a localized lesion in the right peduncle and tegmentum of the midbrain. Single photon emission computerized tomography of the brain using N-isopropyl-P-(123I) iodoamphetamine (IMP) performed about a month after admission disclosed decreased blood flow in the left hemisphere of the cerebellum compared with the right one and the findings of CCD were observed.

Aged↗
PubMed1989

Brainstem auditory evoked potentials in patients with multi-infarct dementia and dementia of the Alzheimer type.

Brainstem auditory evoked potentials (BAEPs) were recorded in 25 patients with multi-infarct dementia (MID) (mean age 71.2 years), 16 patients with dementia of the Alzheimer type (DAT) (mean age 70.6 years), and 34 normal subjects (mean age 69.1 years). Both MID and DAT patients showed significant prolonged interpeak latencies between waves I and V (I-V IPLs) compared to normal subjects (p less than .001 and p less than .01, respectively). In patients with MID, both I-III IPLs and III-V IPLs were significantly longer than those of normal subjects (p less than .01 and p less than .01 respectively). On the other hand, only III-V IPLs were significantly prolonged in patients with DAT (p less than .01). There were no significant differences between MID and DAT with regard to any of the IPLs. Present results suggest that the brainstem lesions are located in the auditory pathways in patients with MID and DAT. However, with BAEP measurements, we were not able to discriminate between patients with MID and DAT.

Aged↗
PubMed1986

[Locked-in syndrome in vascular pathology of the brain].

Seven patients with vascular abnormalities of the brain (infarct of the ventral portions of the pons varolii and/or the midbrain--5, hemorrhage into the base of the pons varolii--1 and transient impairment of the cerebral circulation in the vertebro-basilar system--presented the locked-in syndrome with such underlying disorders as tetraplegia with the maintenance of tendon and the appearance of abnormal plantar muscle reflexes, pseudobulbar syndrome with intact consciousness and the absence of any significant changes in the EEG. Other findings included disorders of eye movement, mainly in the horizontal plane and involuntary muscular activity such as forced crying, decerebrational and decorticational muscular spasms, as well as masticatory automatisms. The authors emphasize the identity of the given syndrome and Filimonov's syndrome which was repeatedly described in Soviet literature before 1966 when the term "locked-in syndrome" was proposed. They also discuss the pathogenetic mechanisms of the development of the locked-in syndrome in occlusion of the basilar artery.

Aged↗