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An 8-year-old boy presented with symptoms compatible with a right internuclear ophthalmoplegia. Magnetic resonance imaging showed a high-intensity signal on T2-weighted images at the level of the medial longitudinal fasciculus. Laboratory evaluation was positive only for sickle cell trait. Sickle cell trait is an uncommon cause for brainstem infarction.
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We have studied three patients with angiographically documented cerebellar venous angioma (CVA). One patient had a subacute cerebellar hematoma and underwent posterior fossa craniotomy for evacuation of the hematoma and excision of the malformation. A hemorrhagic venous infarction of the brain stem and cerebellum occurred, and the patient died three weeks postoperatively. A second patient with an unruptured CVA had a history of headaches, tinnitus, and vertigo. Conservative treatment was elected, and the patient's condition remains unchanged after 11 months of follow-up. The third patient, recently diagnosed as having an unruptured CVA had episodic vertigo and disequilibrium. Conservative treatment was chosen, and he is asymptomatic after six months of follow-up. Based on a review of 24 other cases of CVA plus our experience we could not conclude any definite trend regarding natural history or treatment. However, conservative treatment seems the logical choice in patients with unruptured CVA.
The association of an acoustic neuroma with an ipsilateral venous anomaly or angioma is reported in two patients. In the first, the venous angioma was situated low in the posterior fossa, and was of no significance surgically. In the second, the angioma was strongly attached to the capsule of the tumour. On MRI and angiography the lesion appeared as a large draining vein, encircling the tumour. At operation, extensive dissection of the angioma from the neuroma appeared necessary to prevent venous infarction of the brain stem.
We report here the case of a 32-year-old woman who suffered from a unique angiopathy in the central nervous system (CNS). She died of multiple infarcts in the brain stem and cerebellum during treatment with cyclosporine A after bone marrow transplantation for refractory anemia with excess of blasts. The autopsy findings showed segmental narrowing of the basilar artery, in which circumferential dissection of the internal elastic lamina had occurred. The distal portion of the basilar artery was obstructed by upward dislocation of the dissected intima. Similar angiopathy was also observed at multiple sites along the basilar artery branches. These findings suggest endothelial damage, including vasoconstriction and dissection of the CNS arteries.
The incidence and distribution of ischaemic brain damage in a consecutive series of 151 patients who died as a result of a non-missile head injury in the Institute of Neurological Sciences was determined on the basis of a comprehensive neuropathological and neurohistological examination. Ischaemic damage was identified in 138 cases (91%) even after excluding cases who only had necrosis and infarction related to contusions or fat embolism, and infarction in the brain stem of the type conventionally associated with raised intracranial pressure. The ischaemic damage was assessed as severe in 37 (27%), moderately severe in 59 (43%) and mild in 42 (30%), and in the 138 cases with ischaemic brain damage it was found more frequently in the hippocampus (122 cases; 81%), and in the basal ganglia (119 cases; 79%) than in the cerebral cortex (70 cases; 46%) and in the cerebellum (67 cases; 44%). There were statistically significant correlations between ischaemic brain damage and either an episode of hypoxia or of raised intracranial pressure. From the nature of the brain damage it seems likely that much of it was due to a reduction in the cerebral perfusion pressure. This study has shown that ischaemic brain damage is common after head injury, that at least a proportion of it is probably avoidable, and that it is more important as a cause of mortality and morbidity after head injury than has been hitherto realised.
Venous angioma of the posterior fossa has been described, and the existing literature has been reviewed. The patient presented had a venous angioma located in the pons, and both cerebellar hemispheres and was drained by an enlarged and anatomically anomalous vein within the fourth ventricle. The patient had a "cough headache" and later had signs of cerebellar involvement. A surgical attempt at collapsing the anomalous vein resulted in death in the immediate postoperative period due to venous infarction of the brain stem and cerebellum. Emphasis has been given to the following: 1. "Cough Headache" can be a presenting feature for venous angiomas of the posterior fossa. 2. Venous angiomas of the posterior fossa are developmental anatomic anomalies with enlargement of certain venous structures as a result of inadequate alternative venous drainage. 3. The enlarged vein, which is the pathognomonic feature of venous angiomas, serves a vital function in drainage of blood from structures in the posterior fossa as the usual drainage pathways are inadequate or absent. 4. Operative intervention aimed at resection or collapse of such large veins, which has been successful in treatment of venous angiomas of the frontal lobe, can be disastrous in the treatment of those lesions occurring in the posterior fossa.
A 29-year-old woman who had undergone closure of a secundum-type atrial septal defect using the Amplatzer device 2 years previously developed acute and progressive altered mentation. Initial clinical and imaging data confirmed the diagnosis of multiple cerebral, cerebellar and brain stem emboli, and infarcts. She was treated urgently with an intra-arterial thrombolytic agent with only minimal improvement. Transesophageal echocardiography revealed a large thrombus attached to the left atrial disc of the atrial septal defect occluder, which was the source of the emboli. In conclusion, this is the first reported case, to our knowledge, of disseminated cerebral emboli and infarctions as a late complication of transcatheter closure of a secundum-type atrial septal defect.
Edema disease is a common cause of illness and death loss in pigs during the first 2 weeks after weaning. The disease is an enterotoxemia caused by strains of E. coli that colonize the small intestine and produce Stx2e. Bacterial colonization is mediated by F18ab fimbriae. Susceptibility to disease is determined by presence of receptors for these fimbriae on small intestinal epithelial cells and is inherited as a dominant trait. Clinical signs and lesions are largely the result of Stx2e, which causes necrosis of endothelial and smooth muscle cells in small arteries and arterioles. Vascular damage in the brain stem with resultant infarction and malacia is the main cause of death in affected pigs. Studies conducted by veterinary researchers in the 1950s and 1960s identified the cause of the disease and provided future scientists with hypotheses to test regarding the pathogenesis. In the last two decades, studies using molecular-based techniques have allowed for the definitive identification of bacterial virulence factors that mediate intestinal colonization and vascular damage, that is, F18ab fimbriae and Stx2e. Identification of these virulence factors has provided a basis for current and future development of effective preventative measures, for example, vaccines.
OBJECTIVE: To determine the prognostic significance of spindle coma (SC) according to etiology and EEG reactivity. METHODS: We reviewed 15 patients with SC due to various causes within 8 days of coma to determine the prognostic significance of this EEG pattern. RESULTS: The outcome among survivors was favorable: among 13 survivors, 9 were independent in all activities of daily living (ADLs) at 6 months; 3 were dependent in all ADLs; and one remained in coma. EEG reactivity to noxious stimuli best predicted outcome: All patients (whatever the coma etiology) with EEG reactivity survived; conversely, not all patients without EEG reactivity died. CONCLUSION: In our patients, EEG reactivity independent of etiology predicted survival, neurological examination did not predict outcome. Most SC survivors had a meaningful recovery achieving all ADLs. From the literature, the cause of SC was predictive of outcome: encephalopathy, seizures and trauma had the best prognosis while hypoxia, CRA and structural lesions carried the worst. Literature review revealed that 23% of patients [56/242] died or remained in a persistent vegetative state (PVS). Best outcomes occurred when SC was due to drugs, encephalopathy or seizures: (0/14 died or were in a PVS). With trauma 15% [25/169] died or were in a PVS). Intermediate outcomes occurred with hypoxia and cardio-respiratory arrest (CRA): 33% [7/21] died or were in a PVS. The gravest outcomes occurred with brain-stem and cerebral infarctions, and tumors: 73% [22/30] died or were in a PVS.
Between June 1986 and June 1993 46 different tumors (27 extradural and 19 intradural) located in the petroclival area and/or prepontine cistern have been operated on at The Gruppo Otologico Piacenza and the ENT Department of Bergamo, Italy using a modification of the transcochlear approach. Total tumor removal was obtained in all cases. Complications occurred in eight patients. One patient died due to infarction of the brain stem. The system of modified transcochlear approaches conceived for the removal of various intradural and extradural tumors is presented. This approach, together with its modifications, is the major operative access to the central skull base and clivus among a series of lateral approaches described in the literature. The basilar surgical technique (type A) and its modifications (types B, C, D) are described in detail, and five different, illustrative cases are presented. Indications, limits, results, and complications related to the approach are discussed.
We present a case of a 44-year old male suffering from severe subarachnoid haemorrhage secondary to a ruptured basilar artery aneurysm. Clinical examination on 3 consecutive days fulfilled the criteria for the diagnosis of clinical brain death. Nevertheless, cerebral angiograms showed intracranial filling until the third day after the bleeding. Autopsy showed acute infarction of the brain stem and the cerebellum.
Urinary excretion of catecholamines under insulin hypoglycemia was studied in cerebral infarct patients as well as in patients with Parkinson's disease and subjects with lumbar discopathy (control group). While in the last two categories of subjects a normal response to hypoglycemia, i.e., an increase in urinary excretion of epinephrine was noticed, no such increase was found in patients with cerebral infarction. The disorder is attributed to the unresponsiveness to hypoglycemia of the brain stem centers controlling epinephrine secretion.
Angiography by means of iodinated contrast material, before endovascular or surgical treatment, may result in serious complications in patients with renal insufficiency or previous anaphylactoid reaction to iodine. Alternative techniques, such as magnetic resonance angiography or carbon dioxide angiography, have their own limitations. We report effectiveness and safety of cerebral angiography using gadolinium for a patient with right vertebral artery and basilar artery occlusion and renal insufficiency. A 66-year-old woman with diabetes under medical treatment suffered loss of consciousness and left hemiparesis following dehydration for 24 hours. She was transferred to our hospital. Emergent MRI suggested brain stem and cerebellar infarction due to vertebral artery occlusion with diffusion-perfusion mismatch. Because of renal insufficiency, the digital subtraction cerebral angiography using gadolinium was performed. Appropriate diagnosis was achieved by angiography using gadolinium of 0.4 mmol/kg. There was no any complication including deterioration of renal function. Gadolinium appears to be a safe and useful intraarterial contrast agent in patients with renal insufficiency.
BACKGROUND: The aim of our study was to identify congenital morphological abnormalities of distal vertebral arteries (CMADVA) and their association with cerebral hypoperfusion leading to vertigo, and the role of MR and MRA in the diagnosis of vertebrobasilar (VB) abnormalities. MATERIAL/METHODS: 768 patients who complained of dizziness and/or vertigo were included in the study and evaluated by MR and MRA. CMADVAs were determined in 88 of the cases with no other explanation for vertigo and dizziness. 150 patients without dizziness or vertigo were used as a control group. The 3D TOF (Time- of- flight) MR angiographic technique was used. RESULTS: CMADVAs were detected in 88 of 768 patients (11.5%) with vertigo and/or dizziness. We also detected CMADVAs in 4 (2.7%) of 150 persons in the control group. The patients with abnormal vertebral artery findings were classified into ten categories. Lacunar infarcts in the brain stem were found in 8 patients after long-duration vertigo attacks. There was significant correlation between the control and vertigo groups in terms of CMADVA (p=0.0001). After excluding the control group, there was a significant relationship between CMADVA and vertigo and/or dizziness symptoms (p=0.0001). CONCLUSIONS: We believe that vertigo and dizziness associated with CMADVA is a real entity that deserves greater attention. For this reason, the vertebrobasilar system in these patients should be examined for CMADVA with MRA. This would enable us to take preventive measures against brainstem ischemia or at least elucidate the etiology of vertigo in these patients.
There is a large range of neurologic complications in periarteritis nodosa, but oculomotor motility disorders are rarely seen. Two patients presented with third nerve palsy and one presented with internuclear ophthalmoplegia due to periarteritis nodosa vasculitis. We hypothesize that the third nerve palsy and internuclear ophthalmoplegia was caused by a vascular infarction in the brain stem.
A 60-year-old woman was admitted with congestive heart failure, essential hypertension and abdominal distension. Her son reported that she appeared with red spots in the body and that she was under dapsone therapy. Seven months ago there was sudden increase of the skin lesions. In the 11th day after admission she underwent a stroke that progressed to decerebration and she expired on the fourth day. Autopsy confirmed CHF due to chronic myocarditis related to Chagas' disease. Aneurysm of the apical region of the left ventricular chamber was also observed leading to thrombosis and systemic embolism with brain and spleen hemorrhagic infarct. In the encephalous there was edema, uncus herniation and hemorrhagic infarct of the brain stem. The skin lesions were due to reactional tuberculoid hanseniasis (RHT) with focal lesions in axillary lymphnodes, nasopharyngeal mucosa and in the posterior tibial nerve. The pathogenesis of RHT is discussed as well as its differentiation with the BT group of Ridley and Jopling and its probably relationship with the secondary tuberculoid hanseniasis reported by Ridley. The focal lesions are also discussed with END to the involvement of a peripheral nerve trunk what is said to be uncommon in this form of Hansen's disease.