Peroxidase activity in autopsy material. Evaluation of microcirculation.
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Heavily T2-weighted fluid-attenuated inversion recovery (FLAIR) sequences with inversion times of 2000-2500 ms and echo times of 130-200 ms were used to image the brain stem of a normal adult and five patients. These sequences produce high signal from many white matter tracts and display high lesion contrast. The corticospinal and parietopontine tracts, lateral and medial lemnisci, superior and inferior cerebellar peduncles, medial longitudinal fasciculi, thalamo-olivary tracts and the cuneate and gracile fasciculi gave high signal and were directly visualised. The oculomotor and trigeminal nerves were demonstrated within the brain stem. Lesions not seen with conventional T2-weighted spin echo sequences were seen with high contrast in patients with infarction, multiple sclerosis, sarcoidosis, shunt obstruction and metastatic tumour. The anatomical detail and high lesion contrast given by the FLAIR pulse sequence appear likely to be of value in diagnosis of disease in the brain stem.
The neurologic manifestations most frequently described in association with diabetes are caused by involvement of the peripheral nerves and nerve roots. Whether there is also a specific central nervous system involvement has not been well documented. Pseudotabes diabetica and diabetic amyotrophy probably can be explained on the basis of severe neuropathy or radiculopathy. According to fairly recent studies, however, both myelopathy and encephalopathy may be part of the diabetic process. In the cases of myelopathy, there are degeneration of the long tracts and areas of demyelination with gliosis, as well as microinfarcts. In the cases of encephalopathy, there are degeneration of ganglion cells and nerve fibers in the cerebrum, brain stem, and cerebellum; cell loss, demyelination and gliosis; and infarction secondary to severe angiopathy.
Using a standard protocol including MRI and magnetic resonance angiography (MRA), we studied 28 consecutive patients, all with an acute infarct in the lower brainstem. MRI patterns above and below the inferior olivary nucleus enabled identification of six topographical types of infarct: small midlateral, dorsolateral, inferolateral, large inferodorsolateral, dorsal and paramedian infarcts. Small midlateral, dorsolateral, inferolateral and inferodorsolateral infarcts were the most common types and were associated with Wallenberg's syndrome, with specific clusters and severity of neurological features in each of the four groups. Dorsal infarcts were both anatomically and clinically overshadowed by a constant associated cerebellar infarct in the posterior inferior cerebellar artery (PICA) territory. Paramedian infarction led to crossed tongue and sensorimotor hemiplegia, while a patient with an almost complete hemimedullary infarct had unusual ipsilateral sensory and motor disturbance due to lesion extension toward the upper spinal cord. A coexisting cerebellar infarct was present in 36% of the cases, but was never found with midlateral or inferolateral infarct. Angiography showed an embolic occlusion of the PICA in five patients (18%), four of them having dorsal or dorsolateral infarct. Atheromatosis was by far the most frequent stroke aetiology (72%), with intracranial vertebral artery tight stenosis or occlusion in 28% of the cases and in 75% of the cases with large inferodorsolateral infarct. Vertebral artery dissection and cardioembolism accounted each for 14% of the cases, the latter being associated with dorsal infarct. Our study shows that differences in topographical patterns of infarction in the lower brainstem probably reflect differences in aetiopathogenic mechanisms.
Cerebral edema secondary to ischemia can threaten life, mainly due to frequent failure of medical management. Imminent herniation of the temporal lobe can be timely detected by clinical signs and CT-scan. Eight patients (4M, 4F; 48-74 years, mean 62) with ischemic stroke and imminent herniation, were surgically decompressed by a standard temporal lobectomy as described by Olivier for temporal lobe epilepsy. Six patients survived, two died and were considered failure of the procedure, probably due to late surgical indication. In conclusion, temporal lobectomy is life-saving for patients with large ischemic cerebral infarction with mass effect and deteriorating signs of brain stem compression.
AIMS AND BACKGROUND: Metastasis to the brain from prostate carcinoma is a rare event; it is reported in less than 4% of postmortem examinations. The prevalence of cases detected antemortem is even smaller, and the prevalence of brain stem metastasis as the only site of metastasis has been reported in only two other cases. METHOD: The authors present a third such case. RESULTS: A 55-year-old man, treated for an adenocarcinoma of the prostate (prostatectomy and radiotherapy), started to complain of facial expression disturbances and headaches 2 years later. Physical examination showed a left VII cranial nerve palsy. MRI showed an enhancing mass in the pons. Total body CT was negative. The patient was treated with a course of whole-brain and brain stem radiotherapy following stereotactic biopsy. Four months after radiotherapy, the neurological symptoms had disappeared and the patient died of a myocardial infarct. The systemic disease was still clinically silent. CONCLUSION: Our case involved only brain stem metastasis, probably implicating Batson's direct route of the paravertebral venous pathway.
BACKGROUND AND PURPOSE: Silent infarcts are frequently found on MRIs of brains of healthy elderly persons (aged >60 years). The purpose of this study was to investigate the prevalence and determinants of silent infarcts in a population of patients with clinically manifest vascular disease. METHODS: To detect silent infarcts, MR images were made in 308 participants of the Second Manifestations of ARTerial disease (SMART) study (mean age, 58 years) without prior stroke or transient ischemic attack. These are patients referred to the University Medical Center Utrecht because of atherosclerotic vascular disease. Risk factors were assessed by questionnaire and by physical, ultrasonographic, and laboratory examinations. RESULTS: Silent infarcts were found in 51 patients (17%). Most infarcts (62%) were located in white matter, 20% in basal ganglia, 14% in brain stem and cerebellum, and 4% in cortical area. Categorical determinants for presence of silent infarct(s) that remained (borderline) significant after adjustment for age were hypertension (odds ratio [OR]=2.2; 95% CI, 1.2 to 4.2), abdominal aortic aneurysm (OR=2.4; 95% CI, 0.9 to 6.4), severe renal failure (OR=7.3; 95% CI, 2.1 to 25.2), and hyperhomocysteinemia (OR=2.6; 95% CI, 1.1 to 5.9). CONCLUSIONS: Patients with manifest vascular disease are at risk for silent infarcts at a younger age. In particular, patients with the aforementioned risk factors should be considered for treatment or (secondary) prevention.
Vascular accidents of the cerebellum include heamorrhages and infarctions. These two pathologies share the same clinical symptoms and the same potential severity due to the sudden creation of an expansive cerebellar process (haematoma or infarct). Owing to acute compression of the brain stem and of CSF channels in the posterior fossa, and to the resulting supratentorial obstructive hydrocephalus, cerebellar vascular accidents are acute neurosurgical emergencies. Although the diagnosis and prognosis of the lesions have been transformed by computerized tomography of the brain, they remain extremely serious. This underlines the need for early detection, especially since, unlike vascular accidents of the brain, their functional sequelae after treatment are moderate.
Hearing impairment is a rare but characteristic symptom of vertebrobasilar occlusive disease. Two patients with anterior inferior cerebellar artery (AICA) infarction and hearing loss as presenting complaint, are described. In patient 1 progressive bilateral AICA infarction was caused by occlusion of the basilar artery, verified by transcranial Doppler sonography. Initial dizziness and bilateral hearing loss were followed by ataxia, dysarthria, dysphagia and right facial sensory impairment. Hearing loss improved during the second week, parallel to a temporary partial recanalisation of the basilar artery, but the patient subsequently developed further progressive brain stem symptoms and died. A right-sided AICA-infarction was diagnosed in patient 2. Initial symptoms were right-sided deafness and dizziness. Neurological examination revealed nystagmus, ataxia and involvement of th 5th and 6th cranial nerve. A progressive improvement of hearing loss and total recovery of the other brain stem symptoms was evident. In conclusion every patient with sudden hearing loss should be examined for additional brain stem symptoms since this can be the presenting sign of a life-threatening basilar artery thrombosis.
To investigate the role of brainstem dysfunction in patients with dizziness, Brainstem Evoked Responses were recorded, and results of 100 such cases are presented. The present study further emphasizes the fact that dizziness is a symptom complex and careful evaluation of these patients is necessary. If a systematic approach is used, then a correct diagnosis can be achieved in over 95% of the cases. Vascular insufficiency of the brainstem can present as dizziness and may precede a catastrophic vascular infarction by weeks and months. Early recognition of the problem is of paramount importance, since anticoagulation therapy can be started early or other surgical correctable measures can be undertaken to prevent catastrophic infarction.
Magnetic resonance (MR) and computed tomography (CT) imagings were compared in 121 patients with various neurologic diseases. MR was performed with either 0.15 Tesla resistive or 2.0 Tesla superconducting systems developed by Korea Advanced Institute of Science and Technology (KAIST), using multi-slice spin echo technique with a variety of pulse sequences reflecting proton density, T1 and T2 relaxation times. MR was more advantageous in the detection of the lesions, accurate depiction of the lesion extents, and/or demonstration of anatomic details in sagittal or coronal plane in 36 of the 121 patients. These included white matter diseases, cervical cord tumors, syringomyelia, brain stem tumors, foramen magnum tumor, acute cerebellar infarction, Chiari malformation, isodense subacute subdural hematomas, cavernous hemangioma, A-V malformation with hemorrhage and some unknown pathologies. Even though 2.0T superconducting system showed greater capability of demonstrating the anatomic details and contrast discrimination between normal and abnormal tissues, the ability of MR to separate the tumor from the edema and to differentiate among different pathologic entities remained to be further evaluated. CT was superior to MR in 13 patients with acute intracranial hematomas, small calcific lesions, inflammatory granulomas or meningiomas. CT takes less time and may be preferable in very young or elderly patients. Both MR and CT gave equivalent information in the remaining patients. MR proved to complement CT in the evaluation of many disease entities and may actually supplant CT in some.
Ten minutes of total cerebral ischaemia was produced in normo- and hypoglycaemic rats. The most conspicuous findings were loss of hippocampal (CA-1) pyramidal cells and Purkinje cells, which were most pronounced in the normoglycaemic rats. While pre-ischaemic hypoglycaemia to some extent protected these cells, it led to infarction of severe ischaemic nerve cell changes in the brain stem nuclei and lowered the neurological restitution of the hypoglycaemic animals. The regional damage in these rats, which were kept normotensive after ischaemia, was not due to circulatory insufficiency. However, rats with untreated spontaneous low blood pressure in the early postischaemic period showed multiple small infarcts.
Acute bilateral weakness of the extremities with weakness of the tongue classically signals a medullary lesion. A patient had these signs, but at autopsy, bilateral cortical border-zone infarcts and an entirely normal brainstem were found. This case points out the importance of considering bilateral cortical border-zone infarction in the presence of bilateral motor or sensory signs, especially when there is sparing of facial motor function.
Although old or recent infarcts of a cerebellar hemisphere in the territories of the posterior inferior (PICA), superior, or anterior inferior cerebellar arteries are commonplace autopsy findings, in no case have corresponding clinical symptoms been clearly identified. We have studied three cases, two clinocaopthologically and one clinicosurgically, in which an acute infarct involving only the cerebellum lay in the PICA territory distal to the branches to the medulla oblongata. The clinical manifestations consisted of rotatory dizziness intensified by motion, nausea, vomiting, imbalance, and nystagmus. In two cases, the clinical diagnosis had been a benign labyrinthine disorder. Recognition of a syndrome corresponding to cerebellar infarction in the PICA territory is important insofar as it assists in the differential diagnosis of dizziness. It becomes of crucial importance when cerebellar infarction is the prelude to cerebellar swelling and brain stem conpression leading to coma and death unless surgically relieved.