Biomedical subjects
Publications and source records attributed to E F Wijdicks.
We report a 45-year-old man with fulminant pneumococcal meningitis. Fluid attenuated inverse ratio MR images showed the ravaging consequences of occlusive vasculopathy and a transient purulent basal exudate. Bilateral thalamic lesions may have explained the failure to awaken despite appropriate antibiotic therapy.
BACKGROUND: Patients with cerebellar hematomas may appear stable but may worsen suddenly. Whether certain clinical or CT scan findings predict worsening is not known. METHODS: We reviewed clinical and neuroimaging data in 72 patients with cerebellar hematomas at the Mayo Clinic from 1973 through 1993 to identify predictive features for neurologic deterioration. Patients presenting in coma and patients with vascular malformations or malignancies were excluded. Data were analyzed using chi-square or Fisher's exact test, with calculation of odds ratios with 95% confidence intervals. Multivariate logistic regression analysis was performed on appropriate variables. RESULTS: Thirty-three patients (46%) deteriorated, with a decrease in level of consciousness, new brainstem signs, or worsened motor response on the Glasgow Coma Scale. Clinical and neuroradiologic predictors for neurologic deterioration at p < 0.05 were admission systolic blood pressure greater than 200 mm Hg, pinpoint pupils and abnormal corneal or oculocephalic reflexes, hemorrhage extending into the vermis, hematoma size more than 3 cm in diameter, brainstem distortion, intraventricular hemorrhage, upward herniation, and acute hydrocephalus. Multivariate analysis demonstrated that hemorrhage located in the vermis (p = 0.03) and acute hydrocephalus (p = 0.0006) on admission CT scanning independently predicted deterioration. CONCLUSION: Patients with a cerebellar vermian hematoma or acute hydrocephalus are at high risk for neurologic deterioration. These patients should be carefully monitored and are more likely to require consideration for neurosurgical intervention.
OBJECT: The etiology of spontaneous cervical artery dissection is poorly understood; however, it may involve genetic and environmental factors. The purpose of this study was to determine whether seasonality of spontaneous cervical artery dissection exists. METHODS: The seasonal pattern of spontaneous cervical artery dissection was analyzed in a group of 200 consecutive patients (104 females and 96 males with a mean age of 44.9 years) who were evaluated using the Rayleigh test during the period from 1970 to 1990. The majority of patients resided in the midwestern section of the United States, where large seasonal fluctuations in climate occur. A circannual periodicity was found in the frequency of spontaneous cervical artery dissections with a peak occurring in October (p < 0.02). The seasonal variation was substantial, with approximately 58% more patients suffering a cervical artery dissection during autumn than during other seasons. CONCLUSIONS: A seasonal pattern of spontaneous cervical artery dissection exists with a peak occurring in October. The cause of the seasonality remains to be explained; however, weather- or infectious disease-related factors may provide etiological leads.
OBJECTIVE: To review the diagnostic evaluation and the clinical course of patients with pretruncal nonaneurysmal subarachnoid hemorrhage. MATERIAL AND METHODS: The study population consisted of a consecutive series of patients with a pretruncal nonaneurysmal subarachnoid hemorrhage encountered at Mayo Clinic Rochester during a 6-year interval. We reviewed the clinical manifestations, the neuroimaging characteristics, and the appropriate management. RESULTS: The 15 male and 9 female patients with a pretruncal nonaneurysmal subarachnoid hemorrhage ranged from 3 to 72 years of age (median, 45). Of the 24 patients, 18 had a sudden explosive headache at the time of initial assessment. Ventricular shunting for acute hydrocephalus was indicated in one patient. Neuroimaging studies demonstrated that the center of the hemorrhage was prepontine, and it extended into the interpeduncular or premedullary cisterns. In two patients, a small focal hemorrhage was not noted on an admission computed tomographic scan but was identified on repeated study. A second four-vessel cerebral angiogram, obtained in most patients, showed normal findings in four patients who had had cerebral vasospasm on the first study. In one patient, moderate cerebral vasospasm was found on the second angiogram. No patient had rebleeding. One patient had transient dysphasia associated with cerebral vasospasm after cerebral angiography. Two patients had a family history of aneurysmal subarachnoid hemorrhage. CONCLUSION: The excellent outcome in patients with pretruncal nonaneurysmal subarachnoid hemorrhage is in distinct contrast to the overall somber outcome associated with aneurysmal subarachnoid hemorrhage. A ruptured aneurysm of the posterior circulation may mimic a pretruncal nonaneurysmal subarachnoid hemorrhage and should be excluded on the basis of a technically satisfactory cerebral angiogram.
OBJECTIVE: To determine the clinical course and outcome in patients with a middle cerebral artery (MCA) occlusion and early computed tomographic (CT) scan findings of infarction, particularly relative to age of the patient. MATERIAL AND METHODS: The clinical and neuroimaging features of 42 consecutive patients with MCA occlusion and early CT signs of swelling (within 24 hours after ictus) were studied. CT scans were graded for displacement of the pineal gland and septum pellucidum as well as compression of the frontal horn of the ventricular system. Young adults, defined as younger than 45 years of age, were assessed separately. RESULTS: Overall mortality was 55% in this patient population at risk for further neurologic deterioration. Of the 42 patients, 33 had deterioration-an impaired level of consciousness ensued in 3, a diencephalic herniation syndrome developed in 19, and uncal herniation occurred in 11. Mortality was 70% in these patients with deterioration. Mortality was significantly lower in younger patients with deterioration in comparison with older patients (3 of 11 patients versus 20 of 22; P = 0.00018, Fisher's exact test). Factors predictive of deterioration and poor outcome were older age (more than 45 years) and the presence of hyperdense clot in the MCA on CT scan, in addition to early swelling. CONCLUSION: Deterioration from further brain swelling is common in patients with MCA occlusion and sulci effacement on early CT scan. The outcome is fatal in most patients who deteriorate. Mortality was significantly higher in deteriorating older patients than in younger patients. Clearly defined criteria for decompressive hemicraniotomy in young patients with complete MCA occlusion are needed, preferably derived from a randomized clinical trial.
We report the radiographic findings in a case of histologically proven giant cell (temporal) arteritis coupled with high-grade stenoses affecting the internal carotid and vertebral arteries. The 69-year-old patient sought medical assessment because of transient ischemic attacks. The stenoses, which were extradural just proximal to the dural entry point, were thought to be a manifestation of the giant cell arteritis.
The leading cause of acute neuromuscular weakness in the developed world is Guillain-Barré syndrome (GBS). Mortality rates vary widely. This article discusses the care and management of patients with GBS, with an emphasis on those patients who require admission to an intensive care unit.
Acute bilateral infarcts in the territory of the posterior inferior cerebellum artery are rare and poorly documented in the literature. Thus, this report describes the clinical course and outcome in 3 patients. Although one was associated with coronary artery bypass surgery, the etiology was not known. Despite large territorial infarcts, the patients recovered to ambulation with minimal assistance.
Isolated angiitis of the CNS (IACNS) commonly presents with recurrent ischaemic or haemorrhagic infarcts, but subarachnoid haemorrhage is rare. Three patients with IACNS and subarachnoid haemorrhage are reported. Florid granulomatous angiitis with Langhans and foreign body type giant cells was found at necropsy in a child with sudden death. In two other patients the diagnosis was made angiographically. In one patient multifocal infarcts on MRI became evident one week after subarachnoid haemorrhage despite initial treatment with prednisone. Subarachnoid haemorrhage may be the first presentation of IACNS. Characteristic radiographic findings may allow early diagnosis.
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Some clinicians have challenged the clinicopathologic correlation in patients with brain herniation from acute mass lesions. Earlier studies have questioned the significance of downward displacement of the brainstem in supratentorial herniation. Using recent generation MRI, we studied a patient with an acute hemorrhagic infarction. MRI demonstrated significant compression of the diencephalon with downward displacement of the midbrain and hyperintensity on T2-weighted sequences in the lateral mesencephalon during progression from early diencephalic stage to midbrain upper pons stage of herniation. This is the first intra vitam documentation of diencephalic herniation by MR imaging and confirms rostrocaudal deterioration usually found at autopsy.
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We reviewed predictive factors of poor outcome in pontine hemorrhage in 38 patients admitted to the neurological-neurosurgical intensive care unit. Twenty-one patients died within days of admission (55%). Nine patients were severely or moderately disabled and dependent on others for daily care (24%). Eight patients made a good recovery (21%). Death was significantly more common in patients with a history of hypertension, coma on admission, absent motor response, absent corneal reflex or oculocephalic responses. However, clinical and CT features observed only in patients who died were hyperthermia (core temperature > 39 degrees C), tachycardia (> 110 beat/min), CT evidence of extension into the midbrain and thalamus, and acute hydrocephalus on admission. Good recovery only occurred in patients who were alert on admission and had small unilateral pontine hemorrhages. These clinical profiles should be useful in determining the level of care and future resuscitative efforts.
The natriuretic peptide system consists of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP). The system is implicated in the control of body fluid homeostasis, causes natriuresis and diuresis (ANP and BNP), and regulates vascular tone (CNP). A reciprocal relationship between ANP and endothelin (ET) has been suggested, and earlier studies have documented a possible role of ET in cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). The authors studied plasma ANP, BNP, CNP, and ET for 6 consecutive days in 13 patients with SAH by using radioimmunoassay. The median admission values for ANP were 31.5 pg/ml (range 16.8-323 pg/ml [normal 15 +/- 7 pg/ml]); for BNP, 45.3 pg/ml (range 2.2-80.2 pg/ml [normal 12 +/- 9 pg/ml]); for CNP, 7.7 pg/ml (range < 2-20 pg/ml [normal 5.2 +/- 3 pg/ml]); and for ET, 11 pg/ml (range 6.5-25.1 pg/ml [normal 7.2 +/- 4 pg/ml]). Additional increases (defined as > 100% increase on two consecutive measurements) were noted in ANP (11 patients), BNP (10 patients), and CNP (three patients), and resulted in a negative fluid balance in 10 of the 13 patients. The CNP increased in three of four patients with cerebral vasospasm and in one of nine patients without cerebral vasospasm (Fisher's exact test, p = 0.2). No major fluctuations in plasma ET were noted. In seven patients, the plasma ET level did not increase beyond 10 pg/ml during the days of measurement. In six patients, only an occasional sample showed an increase to a maximum of 25 pg/ml. Changes in BNP, ANP, and CNP were independent of each other. The authors conclude that both plasma ANP and BNP increase after SAH and often result in a negative fluid balance. Plasma ANP and BNP seem differentially regulated in the presence of SAH but not by the level of the plasma ET. The possible role of CNP as a regulatory response to cerebral vasospasm needs further exploration.
OBJECTIVE: To investigate the feasibility of intra-arterial thrombolysis in acute basilar artery thrombosis. DESIGN: We reviewed a consecutive series of patients in whom intra-arterial thrombolysis was performed during the period from 1994 to 1996. MATERIAL AND METHODS: Intra-arterial thrombolysis with urokinase was done in an attempt to recanalize the basilar artery in a series of nine patients with basilar artery thrombosis admitted to the neurologic intensive care unit. At the time of initial assessment, all nine patients had major neurologic deficits attributable to brain-stem ischemia, including two patients with locked-in syndrome. RESULTS: Recanalization of the basilar artery system was successful in seven of the nine patients (a range of 2 to 13 hours after the ictus). Failure to recanalize the basilar artery occurred in two patients, who died after progressing to coma. Complete recovery or only minimal neurologic deficits were demonstrated in five of the nine patients. Despite recanalization of the basilar artery, two patients had no major change in their neurologic function, and both ultimately had severe ataxia and were fully dependent on others. A cerebellar hemorrhage occurred in one patient but without clinical worsening. Two patients had a retroperitoneal hematoma. CONCLUSION: Intra-arterial thrombolysis with urokinase in acute basilar artery occlusion resulted in recanalization in seven of the nine patients (78%). Five of the nine patients recovered fully, including two patients who had had locked-in syndrome. In light of the devastating natural course of acute basilar artery occlusion, these initial results are encouraging and indicate that intra-arterial thrombolysis may be a useful emergency treatment, even in patients with prolonged symptoms of ischemia (up to 12 hours).
OBJECTIVE: To attempt to determine factors that influence outcome in mechanically ventilated patients with ischemic hemispheric stroke. MATERIAL AND METHODS: We reviewed data on 24 mechanically ventilated patients with an ischemic stroke in the territory of the middle cerebral artery, who had been admitted to a medical, neurologic, or neurosurgical intensive-care unit during the period between 1976 and 1994. RESULTS: The circumstances surrounding mechanical ventilation were generalized tonic-clonic seizures or status epilepticus (N = 6), progression to stupor and inability to protect the airway from brain swelling (N = 8), or--most commonly--bilateral pulmonary edema from congestive heart failure (N = 10). Of the 24 patients, 17 patients died (12 of neurologic causes and 5 of cardiac arrest or cardiac arrhythmias). Of the seven surviving patients, however, four with seizures and one with pulmonary edema were functionally independent. CONCLUSION: Three clinical scenarios generally underlie mechanical ventilation in patients with ischemic hemispheric stroke (generalized tonic-clonic seizures, brain swelling, and bilateral pulmonary edema). The outcome in patients with an ischemic hemispheric stroke and a subsequent need for mechanical ventilation is poor; however, survival and independent function are possible if seizures or pulmonary edema prompt ventilatory support.
OBJECTIVE: To describe the circumstances surrounding pulmonary embolism associated with stroke, the prophylactic measures, and the outcome in affected patients. MATERIAL AND METHODS: We studied pulmonary embolism in patients with acute stroke at Mayo Clinic Rochester during a 2-decade period. Medical records of 30 patients with pulmonary embolus after stroke were reviewed. Pulmonary embolus was diagnosed on the basis of pulmonary angiograms, high-or intermediate-probability ventilation-perfusion scans, or autopsy findings. RESULTS: Sudden death occurred in 15 of 30 patients (50%) with pulmonary embolism. In the other 15 patients, pleuritic pain or dyspnea was a major initial symptom. Pulmonary embolism occurred from day 3 to day 120 (median time, day 20) after the ictus. Prophylaxis against deep venous thrombosis was noted in only 4 of 30 patients. Pulmonary embolism was associated with deep venous thrombosis diagnosed clinically or at autopsy in 11 patients, invariably in the paralyzed leg. CONCLUSION: Pulmonary embolism after ischemic or hemorrhagic stroke may defy antemortem diagnosis in half of the affected patients. Pulmonary embolism in patients with acute stroke can be a cause of early mortality (during the first month after the ictus).
Fusiform aneurysms are often asymptomatic, and therefore their actual incidence is unknown. Ischemic stroke has been linked to dislodgment of small thrombi formed inside the aneurysm but is uncommon. This article describes two patients with rapidly fatal infarction in the entire pons, both cerebellar hemispheres, thalamus, and occipital lobes, findings consistent with occlusion of the vertebrobasilar artery complex. In both patients, autopsies revealed a giant fusiform aneurysm of the basilar artery.