Malpractice Litigation Related to Diagnosis and Treatment of Intracranial Aneurysms.

BACKGROUND AND PURPOSE: Approaches to management of intracranial aneurysms are inconsistent, in part due to apprehension relating to potential malpractice claims. The purpose of this article was to review the causes of action underlying medical malpractice lawsuits related to the diagnosis and management of intracranial aneurysms and to identify the factors associated and their outcomes. MATERIALS AND METHODS: We consulted 2 large legal databases in the United States to search for cases in which there were jury awards and settlements related to the diagnosis and management of patients with intracranial aneurysms in the United States. Files were screened to include only those cases in which the cause of action involved negligence in the diagnosis and management of a patient with an intracranial aneurysm. RESULTS: Between 2000 and 2020, two hundred eighty-seven published case summaries were identified, of which 133 were eligible for inclusion in the analysis. Radiologists constituted 16% of 159 physicians sued in these lawsuits. Failure to diagnose was the most common medical malpractice claim referenced (100/133 cases), with the most common subgroups being "failure to include cerebral aneurysm as a differential and thus perform adequate work-up" (30 cases), and "failure to correctly interpret aneurysm evidence on CT or MR imaging" (16 cases). Only 6 of these 16 cases were adjudicated at trial, with 2 decided in favor of the plaintiff (awarded $4,000,000 and $43,000,000, respectively). CONCLUSIONS: Incorrect interpretation of imaging is relatively infrequent as a cause of malpractice litigation compared with failure to diagnose aneurysms in the clinical setting by neurosurgeons, emergency physicians, and primary care providers.

Contextualizing the use of oncologic imaging within treatment phases: imaging trends and modality preferences, 2000-2014.

BACKGROUND: In the present study, we retrospectively evaluated the use of tomographic imaging in adult cancer patients to clarify how recent growth plateaus in the use of tomographic imaging in the United States might have affected oncologic imaging during the same period. METHODS: At a U.S. academic cancer centre, 12,059 patients with dates of death from January 2000 through December 2014 were identified. Imaging was restricted to brain and body computed tomography (ct), brain and body magnetic resonance (mr), and body positron-emission tomography (pet) with and without superimposed ct. Trends during the staging (1 year after diagnosis), monitoring (18-6 months before death), and end-of-life (final 6 months before death) phases were analyzed. RESULTS: Comparing the 2005-2009 with the 2010-2014 period, mean intensity of pet imaging increased 21% during staging (p = 0.0000) and 27% during end of life (p = 0.0019). In the monitoring phase, mean intensity for ct brain, ct body, and mr body imaging decreased by 26% (p = 0.0133), 11% (p = 0.0118), and 26% (p = 0.0008), respectively. Aggregate mean intensity of imaging increased in the 13%-27% range every 3 months from 18 months before death to death, reaching 1.43 images in the final 3 months of life. Patients diagnosed in the final 18 months of life had an average of 1 additional image during both the 3 months after diagnosis (p = 0.0000) and the final 3 months before death (p = 0.0000). CONCLUSIONS: Imaging increased as temporal proximity to death decreased, and patients diagnosed near death received more staging imaging, suggesting that imaging guidelines should consider imaging intensity within the context of treatment phase. Despite the development, by multiple organizations, of appropriateness criteria to reduce imaging utilization, aggregate per-patient imaging showed insignificant changes. Simultaneous fluctuations in the intensity of imaging by modality suggest recent changes in the modalities preferred by providers.

Posterior fossa imaging in 158 children with ataxia.

OBJECTIFS: To propose a MRI cerebellar algorithm that may be applied to guide genetic/malformative or biochemical investigations for patients with cerebellar ataxia. PATIENTS AND METHODS: Cerebral MRI of 158 patients with cerebellar ataxia and no supratentorial abnormality were examined according to a new categorization system based on posterior fossa imaging. The clinical and radiological findings were confronted to biochemical and/or genetic results using the MR cerebellar algorithm. Seven groups of cerebellar MRI pattern were described: vermian dysgenesis (n=27), cerebellar hypoplasia (n=15), hemispheric cerebellar dysgenesis (n=6), unilateral hemispheric atrophy (n=5), global cerebellar atrophy (n=84), signal abnormalities (n=11) and normal MRI (n=10). Cerebellar hypoplasia, vermian dysgenesis and hemispheric cerebellar dysgenesis groups were classified as malformative disorders. Global atrophy and signal abnormality groups were classified as metabolic disorders. RESULTS: In the vermian dysgenesis group, a specific genetic diagnosis was obtained in eight children (8/27) and all of the mutated genes (AHI1 (JBS3), CEP290 (JBS5), TMEM67 (JBS6), and RPGRIP1L (JBS7)) are involved in primary cilia function. In the group of pontocerebellar hypoplasia specific genetic diagnosis was obtained in one patient (PCH2) (1/15). Thus, nine of 42 children classified as malformative disorder had a molecular diagnosis. Global atrophy and signal abnormality groups were classified as metabolic disorders, specific biochemical was obtained in 46/95 children. In global atrophy group, respiratory chain deficiency was diagnosed in 18 children (18/84). In 21 children a congenital disorders of glycosylation type 1a (CDG Ia) was diagnosed (21/84) and infantile neuroaxonale dystrophy (INAD) was diagnosed in one child. In signal abnormalities group, specific biochemical diagnosis was obtained in six out of 11 children, five children with respiratory chain deficiency and one child with sulphite oxidase deficiency. In hemispheric cerebellar dysgenesis and normal MRI groups, no biological diagnosis was found for any of the patients. In the group of unilateral hemispheric atrophy, we hypothesized a clastic prenatal injury. CONCLUSION: The proposed MR cerebellar algorithm was useful to guide genetic/malformative or biochemical investigations, allowing an etiological diagnosis in 55 children.

Neuroimaging and deep brain stimulation.

Deep brain stimulation (DBS) is a new neurosurgical method principally used for the treatment of Parkinson disease (PD). Many new applications of DBS are under development, including the treatment of intractable psychiatric diseases. Brain imaging is used for the selection of patients for DBS, to localize the target nucleus, to detect complications, and to evaluate the final electrode contact position. In patients with implanted DBS systems, there is a risk of electrode heating when MR imaging is performed. This contraindicates MR imaging unless specific precautions are taken. Involvement of neuroradiologists in DBS procedures is essential to optimize presurgical evaluation, targeting, and postoperative anatomic results. The precision of the neuroradiologic correlation with anatomic data and clinical outcomes in DBS promises to yield significant basic science and clinical advances in the future.

1H MRS spectroscopy evidence of cerebellar high lactate in mitochondrial respiratory chain deficiency.

Cerebellar ataxia is known to occasionally occur in the course of mitochondrial disorders. We report on MR spectroscopy (1H MRS) evidence of elevated brain lactate in the cerebellar area of 11 patients with cerebellar ataxia ascribed to mitochondrial respiratory chain deficiency (RCD). 1H MRS spectroscopy evidence of lactate peak was found in the cerebellum of 9/11 cases, while no lactate was detected in the putamen in 8/11. We suggest using 1H MRS in cerebellar atrophy in the diagnosis of mitochondrial RCD.

Performance measures in neuroradiology.

Performance measurement has been added to the Medicare payment scheme as of July 2007. Two performance measures are applicable to neuroradiology, pertaining to brain and vascular imaging in stroke. These measures are early attempts to rigorously define the meaning of effective performance of neuroradiology.

Molar tooth sign and superior vermian dysplasia: a radiological, clinical, and genetic study.

We have identified a group of 13 patients with a homogeneous radiological pattern at MRI consisting of the molar tooth sign (MTS) and superior vermian dysplasia. The patients represent a relatively heterogeneous clinical group with variable severity of developmental delay, ataxia, hypotonia, and apnea. Careful examination of MRI prompted us to split our series of patients into two groups, based on IVth ventricle dilatation. In 4/13 patients the IVth ventricle was judged to be dilated and those patients were less severely affected while most clinically affected patients had a normal IVth ventricle. DNA samples of blood leukocytes from 6/13 consanguineous patients were genotyped using polymorphic markers encompassing the Joubert syndrome loci. We therefore sequenced AHI1 located in 6q23 in two patients who were homozygous at the locus and in four sporadic cases. Only one homozygous nonsense mutation was identified. Clinically, the patient exhibiting the AHI1 mutation was the most severely affected child with a profound encephalopathy, major hypotonia, ataxia, Leber congenital amaurosis, and normal IVth ventricle at the MRI. The present study suggests that the syndrome associating MTS and dysplasia of the superior vermis of the cerebellum is a clinically and genetically heterogeneous entity and that Jouberin (AHI1) mutations account for a marginal fraction of patients.

Parieto-occipital grey matter abnormalities in children with Williams syndrome.

Williams syndrome (WS) is a neurodevelopmental disorder resulting from a hemizygous deletion of chromosome 7q11.23. The phenotype of WS consists of typical dysmorphic features, supravalvular aortic stenosis, infantile hypercalcemia and growth retardation. While language and facial recognition seem to be relatively spared, visuospatial constructive disabilities are a hallmark of the neurobehavioral profile of WS. In order to search for actual structural abnormalities underlying this precisely defined neurodevelopmental disorder, we performed anatomical magnetic resonance imaging (MRI) in 9 WS children (11.6 +/- 3.1 years; age range: 5.5-15 years) and 11 normal age-matched control children (11.8 +/- 2.2 years; age range: 8-15 years) using voxel-based morphometry (VBM). VBM is a fully automated whole-brain technique that delivers a voxel-wise assessment of regional grey and white matter concentration. A significant decrease in grey matter concentration was detected in the left parieto-occipital region of WS children (P < 0.05 corrected height threshold). The location of this abnormality in WS children coincides with the location of the structural abnormality previously described using the same method in 13 WS adults. These parieto-occipital abnormalities are consistent with the cognitive profile of WS which includes severe visuospatial construction and numerical cognition deficits. The demonstration of identical structural abnormalities in both adults and children argues for their early origin. Additionally, our study provides support for the use of advanced structural imaging techniques in children, in order to improve our understanding of neurobehavioral phenotypes associated with well-defined genetic disorders.

Limited ischemic necrosis despite prolonged basilar artery occlusion treated with local thrombolysis: a clinicopathologic study.

Based on published case series, intra-arterial thrombolysis for basilar artery occlusion reduces mortality and improves outcome even when performed after considerable delays. In contrast, the current use of intravenous thrombolysis is limited to a 3-hour time window. The longer time window for intervention in patients with basilar artery occlusion may vary based on individual clinical features, such as collateral circulation and the site of the occlusion. Clinicopathologic evidence is presented from a patient with a distal basilar artery occlusion treated with local thrombolysis who later expired from a myocardial infarction complicated by cardiac tamponade. Autopsy showed infarction limited to the right pons despite symptom duration of over 72 hours and directly observed neurologic deficits for 27 hours.