[Experimental brain stem infarction in the dog. Observation of the course (author's transl)].
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A 53-year-old man was admitted to our hospital for back, left shoulder and upper limb pain. Chest radiography and CT on admission revealed right pleural effusion and a focal plate-like thickening of the major fissure. Pleural effusion cytology revealed adenocarcinoma, which was diagnosed as non-small-cell lung cancer with bone metastasis. The patient suffered from DIC, melena and multiple cerebral infarctions during chemotherapy and died on the eighth day of the second course of chemotherapy. Autopsy revealed a pseudomesotheliomatous adenocarcinoma covering the pleura of the right middle lobe, systemic thromboembolism and vegetations on the aortic valves due to nonbacterial endocarditis. Pseudomesotheliomatous adenocarcinoma of the lung, a rare form of lung cancer, complicated with DIC and nonbacterial endocarditis, is reported.
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We present the case of an isolated inferior oblique muscle paresis from ventral midbrain infarction involving the oculomotor fascicular fibers. Based on this case and a review of the literature, the anatomic organization of the oculomotor nerve fascicles and of the pupillary fibers in the ventral midbrain tegmentum is proposed.
A 59-year-old man had loss of pin-prick and temperature sensation over his head, face, neck, trunk, and all extremities while light touch, vibration, joint position sense, and deep pain were preserved. This was the cumulative result of infarctions in the territories of the right superior cerebellar and left posterior inferior cerebellar arteries that occurred three years apart. To our knowledge, a syndrome of bilateral discrete interruption of spinothalamic tracts and of the spinal tracts of the trigeminal system in the brain stem has not been reported. Dissociated sensory loss enveloping the entire body accompanied by truncal and limb ataxia without weakness demonstrated a striking clinical picture. The preservation of deep somatic and visceral pain when cutaneous pain sensation was lost was another notable feature. We review the causes of widespread dissociated sensory loss and discuss the implications of the dissociation of deep from superficial pain.
Chronic intermittent bipolar electrical stimulation of the left nucleus reticulatus polaris thalami was performed in a patient in a state of subcoma due to ischaemic infarction of wide medial parts of the midbrain, mainly the tegmentum, and the right-sided mediobasal parts of the forebrain. Stimulation immediately resulted in autonomic reactions and behavioural arousal reactions during the periods of stimulation. Longterm effect consisted of a rise in the level of clinical responsiveness for a period of seven weeks. A preexistent severe pneumonia disappeared completely after one week of stimulation and returned after seven weeks. The results are discussed on the basis of the pathoanatomical findings and of the physiological functions of the damaged as well as of the stimulated areas.
The present article describes a patient with ischemia in the vascular territory of the posterior inferior cerebellar artery, who developed in addition to other typical signs of the dorsolateral medulla oblongata, myoclonic movements of the ipsilateral vocal cord. Within a period of one year, the myoclonic movement progressed, leading to bilateral involvement of the velo-pharyngeal muscles. The essential neuropathological lesion is considered to be an impairment of the dentato-olivary System. In this respect there is a close relationship to other types of rhythmical myoclonus due to lesions of the brain-stem and cerebellum.
UNLABELLED: A retrospective study of patients who suffered cerebrovascular accidents (CVA particularly brainstem damage) was conducted to look for risk factors which, present on admission, indicated the chance of survival. The evolution of 100 patients, hospitalized in the Neurology Department, University Hospital Lausanne, after having had their first CVA was studied. The risk factors chosen were age, sex, hypertension, smoker, late onset diabetes, hypercholesterolemia as well as the conscious state, the location of the lesion and whether it was bi- or unilateral. Analysis of the data was performed by means of a stepwise multiple logistic regression program. The results demonstrated that diabetes or bilateral lesions, regardless of their position in the brainstem, or the combination of these two factors, indicated an unfavorable outcome, associated with a short term mortality rate greater than 30%. In their absence and despite the presence of the other risk factors, it was less than 2%. At one month the mortality rate was shown to be very high. At two month it was non insignificant and thereafter it became similar to that of the Swiss population. Brainstem lesions extending to the vital centres or respiratory complications related to the state of dependence were the most common causes of short term deaths. At long term the aetiology of death was the same as for the population as a whole. CONCLUSION: The results obtained show the importance of the prevention and treatment of patients at risk of CVA, particularly diabetes. To avoid the fatal complications, that arise from severe handicap in bedridden patients, the management must be rapid and efficient (physiotherapy and drugs).
FLAIR (fluid-attenuated inversion recovery) images are MR images obtained with an inversion recovery sequence having a long inversion time (TI) and a long echo time (TE). We examined 47 cases (56 graphics) of lacunar infarction (LI), 28 cases (32 graphics) of cortical infarction (CI) and 16 cases (23 graphics) of stem infarction (SI) with a FLAIR sequence having a repetitive time (TR) of 6500 msec, a TI of 1700 msec and a TE of 110 msec, and compared these graphics with T2-weighted images by spin-echo sequence (TR 2500 msec, TE 90 msec). LI and CI were better demonstrated with FLAIR images than with conventional T2-weighted images. FLAIR images were very useful in detecting lesions adjacent to the lateral ventricles and the cerebral sulci in particular, because the cerebrospinal fluid signals in the lateral ventricles and the cerebral sulci were low-intensity, with brain tissue appearing as high-intensity areas. In a number of old infarctions, FLAIR images revealed cystic structures, constructed out of internal low-intensity areas and peripheral high-intensity areas. These structural changes suggested that FLAIR images can provide information on pathological changes.
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Seventy-nine autopsy correlations of CT scans showed (1) excellent correlations in normal brains, but the size of the lateral ventricles consistently larger during life than after death; (2) a distinctive pattern differentiating obstructive from nonobstructive hydrocephalus; (3) infarctions appearing as areas of decreased densities of parenchyma in vascular distributions; (4) distinctive high density appearances of hemorrhages that differentiated them from infarctions and, in general, all other pathologic processes; (5) supratentorial, intraventricular, and posterior fossa tumors appearing as masses that displaced, distorted, collapsed, and enlarged normal spaces and structures such as ventricles and pineal gland; (6) 11 false-negative CT scans in some cases of brain stem infarction, brain stem hemorrhage, and small metastasis; and (7) an overall accuracy of 86.2 percent of CT scanning in correctly identifying pathology of the brain.
Clinical and hemodynamic studies were carried out in 75 patients with stem brain infarction in the acute period, including repeated infarctions. The total rupture of the autoregulatory mechanisms of the brain blood flow was discovered, leading to the development of different phenomena of "brain steal" determining the clinical course of stem brain infarction. In the given pathology, the acute period is characterized by the development of the vicious circle of hemodynamic disorders, which is coupled with pathological dissociation in coagulation hemostasis. The progression of the hemodynamic changes requires pathogenetic correction of central and cerebral circulation.
Three cases of idiopathic brain-stem infarction are added to the literature on 12 children. There is no age predilection, and the youngest case is 3 years old. However, there is a striking male preponderance of 13:2. The residual neurological deficit covers the range of normal to quadriparesis. Laboratory studies investigating hypercoagulopathy, platelet dysfunction and atrial septal defect may provide an etiology for some cases in the future.
In clinical stroke cardiovascular abnormalities are frequently neglected although they occur more often than it is generally assumed. However, cardiac arrhythmias, pathological ECG findings, and changes of circadian blood pressure patterns are significantly increased in patients with acute cerebrovascular lesions and are associated with an increased mortality. Several clinical studies have shown that cerebral infarctions may cause different cardiovascular abnormalities depending on the location and the size of the stroke. Hereby, the prolongation of the QT interval and the expansion of the QRS-complex as the most frequent ECG abnormalities are regarded as indicators of the electrical instability of the ventricular myocardium. Furthermore, cardiac enzyme increases are interpreted as an indicator of myocardial damage during the acute phase after cerebral ischaemia. Since the autonomic nervous system plays a major role in the regulation of blood pressure, alterations of sympatho-adrenergic activity can also affect the diurnal blood pressure profile. Some studies report frequent changes of the circadian blood pressure patterns with a decreased night-time blood pressure decline or a pathological night-time blood pressure elevation. Several studies proved the importance of infarct location. The insular cortex in particular has an important role in the genesis of the pathological activation of the sympathetic nervous system. Hence, a highly significant relationship between the extent of circadian blood pressure variation and percentage insular infarction could be found. Some findings implied that the mechanism of cardiovascular instability following stroke relates to the disinhibition of the insular cortex and a reacting augmentation of the sympathetic tone. A further important aspect is given by the strong evidence that sympathetic activation ] is lateralized following hemispheric brain infarction. Accordingly, patients with a right-sided hemispheric infarction showed a significantly diminished circadian blood pressure variation as compared with patients with left-sided hemispheric infarction. The results in patients with brain stem infarction were heterogeneous. On the one hand, patients with brain stem infarction had substantially higher mean plasma norepinephrine levels than did patients with hemispheric infarction; on the other hand, hemispheric lesions were associated with a significantly higher incidence of cardiac arrhythmias when compared to patients with brain stem infarction.
The authors report 10 patients with progressive neurological deterioration due to massive cerebellar infarctions. Computerized tomography scans confirmed obstructive hydrocephalus and brain stem compression. All 10 patients (seven men, three women; mean age, 59 years) were treated by external ventricular drainage and decompressive suboccipital craniectomy. After discharge from the hospital, they were followed up (23-101 months) and their functional independence was evaluated by the Barthel Index. The condition of three patients with brain-stem infarction had deteriorated despite decompressive surgery. Two of these died during the acute stage and one because severely disabled. The remaining seven patients showed neurological improvement during the postoperative period. Four patients with preoperative Japan Coma Scale of 100 returned to their previous jobs within the follow-up period and three patients with preoperative Japan Coma Scale of 200 required some assistance in daily activities. It is suggested that decompressive surgery may be beneficial for massive cerebellar infarction. The postoperative prognosis depends mainly on the presence or absence of coexisting brain-stem infarction. It is possible that, without brain-stem infarction, patients who remained in a "dependent" state may have recovered better if they had been operated on earlier.
BACKGROUND: Basilar artery occlusion usually has a very poor outcome and is associated with a high mortality rate. Local intra-arterial thrombolysis may improve the clinical outcome and reduce mortality in the treatment of acute basilar artery occlusion. We evaluated the possible variables affecting recanalization and clinical outcome in patients with basilar artery occlusions undergoing thrombolytic therapy. METHODS: We analyzed retrospectively the clinical course and outcome of a series of 26 patients between 1998 and 2001. All patients who were examined within 24 hours after onset of symptoms underwent emergency cerebral angiography and subsequent intra-arterial thrombolysis. Three patients additionally received percutaneous transluminal angioplasty of underlying stenosis at the site of thrombosis. RESULTS: Outcome was good in 9 patients (34.6%) and poor in 17 (65.4%). Recanalization could be achieved in 24 patients (92.3%) and was not affected by age, sex, site of occlusion, etiology, thrombolytic drugs, or time interval. Good outcome was associated with younger age, good initial clinical condition, and no evidence of brain stem infarction. There was no association between the interval (greater or less than 6 hours) from the onset of symptoms until the end of thrombolysis and survival. CONCLUSIONS: We confirm that intra-arterial thrombolysis reduces mortality in basilar artery occlusion. Young patients (<75 years) without any infarct in brain stem before the start of treatment seem to be the ideal candidates for thrombolysis. Basilar artery thrombosis could and should be reopened, even late (after 6 hours) after symptom onset.