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PubMed2000

[A case of brain stem infarction with bilateral hearing loss].

The study case was a 66-year-old man who had bilateral neurosensory hearing impairment due to brain stem infarctions. He noticed mild hearing loss, frequent vertigo and tinnitus. About one month later, his hearing took a sudden turn for the worse, and he suffered from dysarthria, dysphagea and abasia. Neurological examination revealed pseudobulber palsy, left hemiparesis, cerebeller ataxia, disturbance of pain and temperature sensation on the right face and left side of the body. Brain stem auditory evoked potentials (BAEPs) showed a delayed small wave V with the abscence of previous waves on the right side and no significant waves on the left side. Brain magnetic resonance images (MRI) revealed infarctions in the bilateral middle cerebellar peduncles, including in the right lateral portions of pons, and the right lower pontine base. We believe that not only peripheral, but also central auditory pathways adjacent to infarctions were damaged. Magnetic resonance angiography (MRA) showed severe stenosis or occlusion of left vertebral artery and basilar artery. We concluded that hypoperfusion of the vertebrobasilar artery territories caused ischemia of the cochlear nerve and the auditory tracts in the brain stem, which resulted in bilateral hearing loss.

Aged↗
PubMed1976

A quantitative study of the EMI values obtained for normal brain cerebral infarction and certain tumours.

A quantitative study has been made of the EMI numbers of normal brain, cerebral infarction and certain tumours. The scans were recorded on magnetic tape and analysed using a minicomuter linked to a graphic display unit. This system not only yielded 16 grey scales compared with the ten currently available, but was programmed to allow selected regions of the scans to be outlined. From these regions the computer calculated the area, the mean EMI number and its standard deviation. It was found that in 15 normal brain scans, the EMI values obtained for normal frontal and temporal lobes were similar, but that the values for the basal ganglia and occipital lobes were significantly different from the first two regions and from each other. Ten cases of cerebral infarction and 30 cases of cerebral tumour were analysed, and it was shown that analysing representative areas was more informative than surveying the whole lesion. Whilst only half of the scans of brain tumours had a significantly altered EMI number compared with that of normal brain, enhancement of tumour density with sodium iothalamate revealed a consistent and significant elevation of the EMI number for all tumours. In particular, the value for enhanced meningiomas was almost double and malignant tumours more than a third larger than normal brain. It was not possible to differentiate quantitatively between astrocytomas and metastases.

Brain↗
PubMed1990

Cerebrovascular accidents in infective endocarditis: role of anticoagulation.

Anticoagulation is still a matter of debate in infective endocarditis, since it can increase the risk of complications, mostly neurological. In our series of 269 patients with native valve endocarditis studied between 1970 and 1982, 35 were anticoagulated. We observed 14 patients with brain infarcts, of whom five died, and 12 patients with cerebromeningeal or brain haemorrhage of whom six died. In a similar series of 63 patients with prosthetic valve endocarditis, all of whom were on anticoagulation and were studied between 1972 and 1987, we observed five patients with brain infarcts, three of whom died, and two patients with brain haemorrhage, one of whom died. The frequency of cerebrovascular accident (CVA) was similar for both groups (11.1% in prosthetic endocarditis vs 11.5% in native valve endocarditis, P = ns), as was mortality rate (57% vs 48.4%, P = ns). CVA are significantly more frequent among anticoagulated patients (19/94 vs 19/238: P less than 0.01), but the mortality rate in CVA is similar for anticoagulated and non-anticoagulated patients (11/19 vs 8/19: P = ns). The indications for anticoagulation in infective endocarditis remain similar to those in valvular heart disease. In patients with infective endocarditis, anticoagulation with heparin should be maintained whenever a brain infarct is present, unless it is large and/or haemorrhagic.

Adolescent↗
PubMed2001

Time course of lesion development in patients with acute brain stem infarction and correlation with NIHSS score.

BACKGROUND AND PURPOSE: diffusion weighted magnetic resonance imaging (MRI) is highly sensitive in detecting acute supratentorial cerebral ischemia and Diffusion Weighted Imaging (DWI) lesion size has been shown to correlate strongly with the neurologic deficit in middle cerebral artery territory stroke. However, data concerning infratentorial strokes are rare. We examined the size and evolution of acute brain stem ischemic lesions and their relationship to neurological outcome. METHODS: brain stem infarctions of 11 patients were analyzed. We performed DWI in all patients and in 7/11 patients within 24 h, T2W sequences within the first 2 weeks (10/11 patients) and follow-up MRI (MR2) within 3-9 months (median 4.8 months) later (12/12 patients). Lesion volumes were compared with early and follow-up neurologic deficit as determined by National Institutes of Health Stroke Scale (NIHSS) score. RESULTS: the relative infarct volumes--with MR2 lesion size set to 100%--decreased over the time (P<0.02) with a mean shrinking factor of 3.3 between DWI (MR0) and the follow-up MRT (P<0.02), and 1.6 between early T2W (MR1) and MR2 (P<0.04). The mean DWI volume size (MR0) was larger than the early T2W (P<0.02). Although neurological outcome was good in all patients (mean NIHSS score of 1.3 at follow-up), early NIHSS and follow-up NIHSS scores were strongly correlated (r=0.9, P<0.00). NIHSS score at follow-up was highly correlated with lesion size of DWI (MR0; r=0.71, P<0.04) and T2W of MR1 (r=0.86, P<0.001). CONCLUSIONS: in this study, we saw a shrinking of the brain stem infarct volume according to clinical improvement of patients. Great extension of restricted diffusion in the acute stage does not necessarily implicate a large resulting infarction or a bad clinical outcome.

Brain Stem Infarctions↗
PubMed1996

Diabetes and brain ischemia.

Diabetes influences brain ischemia in a number of different ways. Diabetes causes and exacerbates macroangiopathies, increases the severity of ischemia, and increases stroke mortality. Unfortunately, few studies have examined in sufficient depth the influence of diabetes on the various vascular lesions that cause brain ischemia. These can be divided into: 1) cardiac-origin brain embolism; 2) atherosclerosis of the aorta and the large extracranial arteries--the internal carotid arteries (ICAs) and the vertebral arteries (VAs); 3) atherosclerosis of the large intracranial arteries--ICAs, anterior, middle, and posterior cerebral arteries, the VAs, and the basilar artery; 4) intracranial atheromatous branch disease of macroscopically visible branches of the intracranial arteries enumerated in 3; and 5) degenerative abnormalities such as lipohyalinosis and fibrinoid changes within penetrating artery branches visible only microscopically. The last three types of disorders all can cause deep subcortical brain infarcts, the predominant type of brain infarction found in Japan.

Brain↗
PubMed1991

Increase in cerebrospinal fluid and plasma levels of 3-methoxy-4-hydroxyphenylglycol in acute stroke.

BACKGROUND AND PURPOSE: 3-Methoxy-4-hydroxyphenylglycol is known to be a principal metabolite of brain norepinephrine and to be released into the blood and cerebrospinal fluid in association with activation of the central noradrenergic system. We examined changes in plasma and cerebrospinal fluid levels of 3-methoxy-4-hydroxyphenylglycol during acute stroke to see if there might be a correlation between these and the patient's clinical state. METHODS: We measured plasma levels of 3-methoxy-4-hydroxyphenylglycol in 32 control subjects and in 50 patients with brain hemorrhage and 57 patients with brain infarction who were admitted to the hospital within 72 hours after onset. In addition, we estimated 3-methoxy-4-hydroxyphenylglycol concentrations in the cerebrospinal fluid of 37 patients with brain infarction and eight control patients. RESULTS: Mean +/- SEM values for plasma 3-methoxy-4-hydroxyphenylglycol in the patients with brain hemorrhage and those with brain infarction were 7.3 +/- 0.5 and 6.6 +/- 0.5 ng/ml, respectively. Both values were significantly higher than that obtained in the 32 control subjects (4.6 +/- 0.3 ng/ml, p less than 0.01). Plasma levels of 3-methoxy-4-hydroxyphenylglycol correlated well with state of consciousness and prognosis. The mean +/- SEM level of 3-methoxy-4-hydroxyphenylglycol in the cerebrospinal fluid of the 37 patients with brain infarction (10.9 +/- 0.6 ng/ml) was also significantly higher than that in the eight control patients (7.9 +/- 0.6 ng/ml, p less than 0.01). CONCLUSIONS: The observed increase in plasma and cerebrospinal fluid levels of 3-methoxy-4-hydroxyphenylglycol implies that the activity of the central noradrenergic neurons may be enhanced at the onset of stroke, and these levels may be related to some extent to the clinical state and prognosis of stroke patients.

Aged↗
PubMed1992

Pediatric brain stem infarction caused by a basilar and vertebral artery occlusion: case report.

Basilar and right vertebral artery occlusion, which caused a brain stem infarction, occurred in an 11-year-old boy. There have been nine previous cases of basilar artery occlusion with steno-occlusive lesion in the vertebral artery. It is suspected that dissection of the vertebral artery at the atlantoaxial level and a gradual progression of arterial dissection to the basilar artery were the major causes of this infarction.

Brain Stem↗
PubMed1981

[Cerebrospinal fluid chlorine-soluble proteins and lipoproteins in the differential diagnosis of cerebral infarct and brain tumor].

Results of determining the chemical composition and the electrophoretic spectrum of chlorine-soluble proteins and lipoproteins in the cerebrospinal fluid of patients with cerebral infarctions and brain tumours are presented. The determinations showed non-identity of those proteins in the patients with the above diseases. The information obtained can be of value for solving a number of questions concerning the differential diagnosis, determination of the tumour character, as well as some other questions.

Brain Neoplasms↗
PubMed1995

Strokes mimicking peripheral nerve lesions.

Sensory-motor deficit in a peripheral nerve pattern due to brain lesion is rarely documented. We report on seven patients with a clinical manifestation of sensory-motor deficit, imitating peripheral nerve involvement, due to lacunar brain infarcts verified by brain computed tomography scan. Five of the patients had an ulnar nerve-like deficit and two median nerve-like deficits. The infarcts were located in the thalamus and the corona radiata. No clinical or electrophysiological evidence for peripheral nerve involvement was found. The unusual peripheral nerve pattern of lesions caused by lacunar brain infarcts can be defined as an additional lacunar syndrome and must be taken into consideration in the clinical evaluation of peripheral nerve deficits with normal nerve conduction velocity.

Aged↗
PubMed1990

[A case of brain stem infarction with bilateral hearing impairment and tinnitus at the onset].

We reported a 49-year-old male with brain stem infarction who had bilateral hearing impairment and tinnitus at the onset and subsequently developed various neurological symptoms, including bilateral lateral inferior pontine syndrome, one and a half syndrome and upward gaze palsy. Although CT scan failed to reveal any abnormalities initially, MRI revealed symmetrical foci bilaterally from the lateral inferior pons to the middle cerebellar peduncle, as well as in the paramedian portion of the mid-pons. Cerebral angiography: The left vertebral artery (VA) occluded at the 4th segment. The right VA showed severe stenosis at the 4th segment. The basilar artery (BA) was found to be occluded in the lower 1/3 below the clivus. Furthermore, CAG demonstrated upper portion of the BA, bilateral superior cerebellar artery and posterior cerebral artery via the posterior communicating artery, but the bilateral anterior inferior cerebellar arteries (AICAs) were absent or occluded. Neuroradiological findings suggested ischemia in the bilateral AICA and the middle portion of the BA. Bilateral hearing impairment rarely accompanies cerebrovascular disorders. This case of bilateral hearing impairment, tinnitus at the onset, followed by bilateral lateral inferior pontine syndrome was considered to be an extremely rare pathological condition.

Brain Stem↗
PubMed1995

[Results of magnetic resonance imaging in the acute phase of cerebral infarction].

Brain ischemia is now possible to trace through the multiple facets of MRI, morphological as well as functional. Experimental studies have been conducted for many years and clinical feasibility is reached. Although the initial decrease in blood flow does not influence morphological imaging, this early phase is shown with functional MRI, either with diffusion imaging or with cerebral blood volume imaging. The later is achieved either with the calculation of the integral of the first passage of a bolus of a diffusible paramagnetic agent or with the circulation of positive or negative blood pool contrast agents. This may serve to confirm an early diagnosis before inclusion in therapeutic trials. Immediate metabolic changes are reflected on phosphorus and proton spectroscopy achievable during the same session as imaging. This type of information may at this stage serve as a reference. It allows observation of the turnover of lactate over time in the lesion and the neuronal loss shown by decreased N-acetyl-aspartate. Edema, as a reaction to ischemia, builds up over time and has already been described for long as it modifies T1- and T2- weighted sequences. Similarly the breakdown of the blood-brain barrier is well known on conventional sequences because it produces contrast enhancement.

Acute Disease↗
PubMed2001

Brain CT infarction in patients with carotid atheroma. Does it predict a future event?

BACKGROUND: The aim of the present study was to investigate the predictive value for subsequent stroke of different patterns of brain CT infarction in patients with carotid atheroma. METHODS: Prospective study on 138 patients, with 138 carotid plaques, having, on presentation, a greater than 50 percent stenosis on duplex scanning and associated with an ipsilateral (to the plaque) amaurosis fugax (AF), hemispheric transient ischaemic attack (HTIA) or which were asymptomatic. This carotid artery defined the side of interest. All patients had a brain CT scan on presentation and subsequently were followed for a period of 1-5 years (mean 3.14). The baseline CT neurovascular findings on the side of interest were classified as pattern A (discrete subcortical and cortical infarctions), pattern B (haemodynamic infarctions, widespread white matter lesions, basal ganglia infarctions and lacunae) and normal CT. RESULTS: On follow-up, 5/27 (18.5 percent) of patients with pattern A, 4/38 (10.5 percent) with pattern B and 3/73 (4.1 percent) with normal CT appearance developed stroke in the hemisphere of interest (Cox regression: p=0.02). CONCLUSIONS: Pattern A confers an unfavourable prognosis in patients with carotid atheroma who are either asymptomatic or presented with amaurosis fugax or hemispheric transient ischaemic attacks.

Adult↗
PubMed1996

Automated measurement of infarct size with scanned images of triphenyltetrazolium chloride-stained rat brains.

BACKGROUND AND PURPOSE: The extent of brain infarction after local cerebral ischemia is frequently assessed with the mitochondrial activity indicator 2,3,5-triphenyltetrazolium chloride (TTC). We describe an automated procedure for analysis of infarct size in TTC-stained rat brains. METHODS: Rats were subjected to middle cerebral artery occlusion and killed after 24 to 36 hours, and their brains were processed for TTC staining. Digital images of coronal sections from these brains (n > 50) were acquired with a desktop color scanner. The resulting images were divided into red, blue, and green component images. Total brain and infarct areas were automatically determined on the basis of total pixel intensity and area after segmentation of the red and green images, respectively. Automated measurements were compared with those made with a video camera-based image acquisition system that required manual tracing of lesion boundaries. RESULTS: The spatial resolution of scanned brain images (approximately equal to 200 microns) was comparable to that of the camera-based system and provided sufficient detail to recognize infarct boundaries and neuroanatomical features. Scanner-based acquisition and analysis were faster than with the camera-based method. The green component image accurately distinguished infarcted from normal brain, and the red component image represented total brain dimensions. Infarct measurements obtained by the automated method correlated closely with those from conventional apparatus (R2 = .89, P < .001). Intraobserver reliability with the automated method (R2 = 1.00) was higher than with the conventional method (R2 = .77). CONCLUSIONS: Infarct size after middle cerebral artery occlusion in the rat can be rapidly and reproducibly assessed with inexpensive scanning equipment and automated image analysis of TTC-stained brains.

Animals↗
PubMed2006

Ischemia-modified albumin in acute stroke.

BACKGROUND: Ischemia-modified albumin (IMA)is a new biological marker of ischemia. Previous studies have found increased serum IMA levels after myocardial ischemia, but no study has investigated the possibility that stroke modifies IMA blood levels. MATERIALS AND METHODS: We studied 118 consecutive patients presenting within 3 h of the onset of an acute neurological deficit [84 brain infarctions (BI), 18 brain hemorrhages (ICH) and 16 transient ischemic attacks lasting less than 1 h or epileptic seizures]. Serum samples were obtained for all patients at initial presentation and repeated only in patients with stroke at 6, 12 and 24 h. IMA was measured by the albumin-cobalt-binding test (Ischemia Technologies, Denver, Colo., USA). RESULTS: The initial median IMA (bootstrap 95% confidence interval, CI) was 83 U/ml (79-86) and 86 U/ml (75-90) in patients with BI and ICH, respectively (p = 0.76), and was 73 U/ml (58-79) in others (p = 0.003 compared with BI, and p = 0.017 with ICH). Baseline IMA levels correlated with the National Institutes of Health Stroke Scale [Spearman correlation coefficient: 0.34 (p = 0.002) in BI, 0.61 (p = 0.008) in ICH]. During the first 24 h, IMA levels increased in BI patients (median, 9.1%; bootstrap 95% CI, 5.2-11.5), whereas no change was observed in ICH patients (median, 1.2%; bootstrap 95% CI, -7.8 to 6.8). CONCLUSIONS: IMA blood levels may be a biomarker for early identification of acute stroke. Further studies are required to investigate the role of IMA in the early detection of acute stroke.

Acute Disease↗
PubMed2005

Familial hypercholesterolemia patients treated with statins at no increased risk for intracranial vascular lesions despite increased cholesterol burden and extracranial atherosclerosis.

BACKGROUND AND PURPOSE: To correlate known vascular disease risk factors and the signs of extracranial and intracranial changes of vascular origin in young patients with heterozygous familial hypercholesterolemia (FH). METHODS: 39 DNA test-verified heterozygous FH North Karelian patients (FH-NK), aged 6 to 48, 28 of them treated with statins, and 25 healthy controls underwent brain magnetic resonance imaging (MRI) and carotid ultrasound. RESULTS: Common carotid intima-media thickness was significantly greater in the patients (P=0.005). MR angiography showed no pathological changes, other than 1 incidental aneurysm. The number and size of white matter hyperintensities on T2-weighted MR images, considered as markers of microvascular alterations, did not differ between patients and controls. CONCLUSIONS: FH-NK patients treated with statins seem to be at no increased risk for brain infarcts or other brain lesions of vascular origin when younger than age 50.

Adolescent↗
PubMed2002

Risk factors for cryptogenic ischaemic stroke.

This case-control study was designed to identify risk factors for cryptogenic brain infarction. We assessed the frequency of prothrombotic states, homocysteine, lipoprotein (a) [Lp(a)] and other lipids and the apolipoprotein E phenotype together with conventional risk factors in 46 patients (19 women and 27 men) with cryptogenic brain infarction aged from 15 to 60 years and in 104 community-based controls. Multivariate odds ratios (ORs) for risk factors and 95% CIs were calculated by logistic regression. Hypertension (OR 4.5; 95% CI, 1.5-13.2; P = 0.006), current smoking (OR 2.9; 95% CI, 1.2-6.8; P = 0.012), low HDL cholesterol (HDL-C) (OR 5.4; 95% CI, 1.1-25.5; P = 0.035) and high clotting factor VIII activity (OR 3.6; 95% CI, 1.1-12.2; P = 0.041) were variables associated with cryptogenic brain infarction. These risk factors were not equally frequent in women and men. Low HDL-C and high factor VIII activity in the women, and hypertension, current smoking and a low level of plasma folate in the men were risk factors for cryptogenic stroke. Several of the observed risk factors for cryptogenic brain infarction were lifestyle-associated, which emphasizes the role of health education in addition to pharmacological treatment in the prevention of stroke.

Adolescent↗
PubMed1986

[Superficial temporal to superior cerebellar artery anastomosis for rostral brain stem infarction].

The authors report a case of superficial temporal to superior cerebellar artery anastomosis (STA-SCA anastomosis) for progressing rostral brain stem infarction with an excellent result. Precise operative techniques were also described. A 47-year-old male was admitted to our hospital on November 9, 1984, because of sudden onset of dysarthria and ataxic gait. CT revealed a low density area in the pons. Left vertebral angiogram showed occlusion of the left vertebral artery just distal to the origin of the posterior inferior cerebellar artery (PICA). Arterial branch of the left cerebellar hemisphere were filled via the left PICA to the left SCA and anterior inferior cerebellar artery anastomosis. Right brachial angiogram showed the hypoplastic right vertebral artery which ended at the PICA. The rostral basilar artery, both posterior cerebral arteries (PCA's) and right SCA were filled through anastomosis from the right PICA. The posterior circulation was not filled by either of the carotid arteries. In spite of antiplatelet agglutination therapy, the patient had two more episodes of dysarthria, dysphagia, right hemiparesis and gait disturbance. Because of progressing stroke, STA-SCA anastomosis was carried out on the right side on February 27, 1985. During operation, the blood pressure was maintained above the level of 130 mmHg, and intravenous mannitol injection and spinal drainage were done to preserve the right temporal lobe from intracerebral hematoma and/or edema caused by retraction. Postoperatively, the patient has been free from new ischemic attack. He has only slight hemiparesis now eight months after operation. Right external carotid angiogram showed a patent STA-SCA bypass and good filling of SCA's and PCA's bilaterally.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain Stem↗