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. 2018 Oct 15;9(2):93–99. doi: 10.1177/1941874418805339

Distinctive FDG-PET/CT Findings in Acute Neurological Hospital Care

Josef G Heckmann 1,✉, Wolfgang Niedermeier 2, Markus Büchner 3, Bernhard Scher 3
PMCID: PMC6429674  PMID: 30915187

Abstract

A compilation of 6 distinctive 18F-fluorodeoxyglucose positron emission tomography (PET) combined with computed tomography (CT) findings in the acute setting of neurohospital care is presented. In case 1, PET/CT allowed the final diagnosis of circumscribed ischemic infarction by demonstrating a clear pattern of luxury perfusion. In case 2, diagnosis of thalamic abscess was made, whereby PET/CT demonstrated an empty zone. Hypermetabolic enlarged hilar lymph nodes and hypermetabolic spinal lumbar roots in PET/CT led to the diagnosis of neurosarcoidosis in case 3. In case 4, a hypermetabolic brain focus in PET/CT identified the seizure focus in epilepsia partialis continua. A cerebral hemispheric hypometabolism in PET/CT in case 5 supported the diagnosis of Creutzfeldt-Jakob disease, which initially mimicked acute stroke. In case 6, PET/CT detected infective endocarditis as a source of multiple cerebral ischemic lesions. In conclusion, PET/CT can contribute importantly to find the correct diagnosis in acute neurohospital patients.

Keywords: 18F-fluorodeoxyglucose positron emission tomography, stroke, CNS infection, epilepsia partialis continua, Creutzfeldt-Jakob disease

Introduction

18F-Fluorodeoxyglucose (FDG) positron emission tomography (PET) is a highly sophisticated method in differentiating various cerebrovascular, neurodegenerative, neoplastic, infectious, or inflammatory diseases. Mostly it is used in nonacute patients such as for diagnosing dementia or characterization of tumorous processes.1-5 Another important focus of this method is its application in studies with neuroscientific questions including consciousness, coma, and vegetative state.2,6,7 Recently developed hybrid imaging of PET combined with computed tomography (PET/CT) allows more detailed anatomical information in detecting malignancies, large-vessel vasculitis, or disease processes in patients with fevers of unknown origin.8,9 In acute clinical neurological care, PET/CT examinations are usually subordinated for different reasons such as availability, logistic efforts, time consumption and timeliness, requirements of extensive facilities and technical support, financial costs and patients’ capacity to cooperate.10,11 Positron emission tomography/CT findings in acute neurological hospital care are therefore sparsely reported.9,12 By presenting a compilation of 6 case vignettes with distinctive PET/CT findings in an acute neurological hospital care, we wish to emphasize that PET/CT is a feasible method which can contribute substantially to find the correct diagnosis.

Clinical Presentation and Comment

Description of Applied PET/CT-Method

After the PET/CT indication was set, informed consent of the patient or his legal representative was obtained. The procedure was performed according the standard operation procedure (SOP) protocol of the Department of Nuclear Medicine, Municipal Hospital Landshut, Germany. This SOP is aligned with the recommendations of different nuclear medicine societies.13 In particular, emphasis was put on a fasting period of at least 4 to 6 hours, sufficient hydration, restriction of physical activity, or exercise prior to the examination, and normal glucose level. A sedative premedication of lorazepam was allowed. In patients with diabetes, a glycemic control with a blood glucose level <200 mg/dL was ensured. Depending on the body weight and length 180 to 250 MBq 18F-FDG was injected. Furosemide (20 mg) was administered to accelerate biological tracer excretion. For CT, a native low-dose CT was used. In addition to the visual evaluation, standardized uptake values were used.

Patient 1

An 82-year-old man was admitted due to acute aphasic symptoms and right-sided weakness, particularly in the leg. An electrocardiogram showed new atrial fibrillation. His first CT scan of the head, and even a second one, did not demonstrate cerebral infarction. Magnetic resonance imaging (MRI) was not done due to a previously implanted pacemaker. Lumbar puncture was normal. As at the same time, weight loss, night sweating, malaise, and elevated laboratory results (liver enzymes, C-reactive protein (CRP), LDH) had been noted, whole-body PET/CT was indicated in search for unknown malignancy or large-vessel arteritis.14,15 In the clinically assumed regions of cerebral infarction, pronounced hypermetabolism was found (Figure 1). This was evaluated as luxury perfusion, confirming the diagnosis of acute embolic cerebral infarction in the territory of the anterior cerebral artery and part of the middle cerebral artery. Finally, additional subacute cholecystitis as the source of weight loss, night sweating, and malaise was treated conservatively.

Figure 1.

Figure 1.

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Panel A. 18Fluorodeoxyglucose-PET/CT shows hypermetabolism due to luxury perfusion in the territory of anterior cerebral artery (white arrows) and in the frontal territory of middle cerebral artery. Panel B. The corresponding CCT at this time only shows slight hypodense changes (arrow) in the territory of anterior cerebral artery (fogging effect). CT indicates computed tomography; PET, positron emission tomography.

Luxury perfusion describes an overabundant cerebral perfusion after an insult. In this region, the perfusion is far more as metabolically needed. Acidosis of the brain parenchyma, disturbed cerebrovascular autoregulation, and reduced oxygen extraction during the blood passage in the infarcted tissue are all discussed as pathophysiological factors.16 Increased glucose metabolism occurs also in tumorous and inflammatory processes. In our case, it is noteworthy that due to fogging effect, the infarction could not be delineated by cranial CT.17 However, by PET/CT, a clear vascular pattern of luxury perfusion could be established and confirmed the diagnosis of cerebral infarction.

Patient 2

A 54-year-old otherwise healthy woman presented with a right-sided sensory and motor syndrome. Computed tomography and MRI of the head showed a lesion in the left thalamic region with slight contrast enhancement and edema. However, as both, cranial computed tomography (CCT) and MRI, could not clear the underlying pathology, cranial PET/CT was pursued. It demonstrated an FDG-negative round-shaped lesion (“empty zone”) without wall uptake (Figure 2) compatible with an abscess which was finally treated by stereotactic abscess drainage and antibiotic regimen. This case was previously reported in detail.18

Figure 2.

Figure 2.

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18Fluorodeoxyglucose-PET/CT scan shows an “empty zone” in the left thalamic region which was finally diagnosed as abscess and treated neurosurgically (discussion of clinical details in Heckmann et al, 2017).18 CT indicates computed tomography; PET, positron emission tomography.

Patient 3

A 65-year-old woman was admitted due to mental confusion, dysphasia, hemianopia, and continuous myoclonic jerks of the right face and upper limb lingering for 5 weeks. The CCT was normal. Cerebral MRI showed initially on a diffusion-weighted sequence a slight hyperintense signal in the left posterior brain (Figure 3A). Cerebrospinal fluid (CSF) analysis showed a slight lymphocytic pleocytosis (17 cells/µL; normal <4), elevated protein (972 mg/L; normal <450) and a transient slight elevation of protein 14-3-3. Cerebrospinal fluid levels of glucose (60 mg/dL) and lactate (2,1 mmol/L) were normal. The results for neurotrophic viruses and bacteria were negative. Autoimmunological screening including antineuronal and paraneoplastic antibodies was normal. Thoracic and abdominal CT revealed an enlarged calcified myomatous uterus but no malignancy. As the diagnostic criteria for possible paraneoplastic encephalitis were present,19 whole-body PET/CT was indicated to search for unknown malignancy or metastasis of previous breast cancer. Positron emission tomography/CT was performed during patient’s ongoing ictal status (epilepsia partialis continua, formerly Kozhevnikov epilepsy). It showed hypermetabolism in the left posterior brain region and the ipsilateral thalamus (Figure 3B). Electroencephalogram (EEG) showed continuous left-sided periodic lateralized epileptiform discharges. Eventually, the epileptic status was terminated after a combined therapy (lacosamide, valproic acid, lorazepam, topiramate). After an intense rehabilitation, the patient recovered partially but died some months later. An autopsy was not performed, and an ultimate diagnosis could not be made.

Figure 3.

Figure 3.

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Panel A. Cerebral MRI (diffusion-weighted sequence) shows a slight hyperintense signal in the left posterior brain (white arrow). Panel B. 18Fluorodeoxyglucose-PET/CT during status of epilepsia particalis continua shows hypermetabolism involving left posterior hemisphere including left thalamus (white arrows). MRI indicates magnetic resonance imaging.

Epilepsia partialis continua is often cryptogenic and difficult to treat.20 The ictal PET/CT findings of hypermetabolism in the left posterior brain regions and the thalamus of our patient did not correlate with the vascular territories excluding cerebrovascular disorder. Moreover all diagnostic procedures performed before PET/CT did not reveal other causes such as tumour, metastasis, inflammation, and infection. Therefore, combined hypermetabolism and focal EEG hyperactivity, both in the left posterior brain, were interpreted as hyperexcitation during and due to ictal status.

Patient 4

A 37-year-old woman complained of back pain, distal paraesthesia in all extremities and a feeling of belt-shaped pressure around her abdomen as well as facial palsy, unsteadiness, and hearing impairment for 5 weeks. Spinal and cerebral MRI was unremarkable. The CSF analysis showed a slight lymphocytic pleocytosis (44 cells/µL; normal <4) with elevated protein level (989 mg/L; normal <450). Treatment regimens on neuroborreliosis and Guillain-Barré syndrome were not successful. To rule out paraneoplasia, whole-body PET/CT was performed. It provided the cue to sarcoidosis because of pathological glucose uptake in mediastinal lymph nodes (Figure 4A) and to neurosarcoidosis because of pathological glucose uptake in thoracolumbar spinal ganglia (Figure 4B). A chest X-ray prior to PET/CT was diagnostically not contributing, a diagnostic body CT was not performed at this time but later confirmed the lymphadenopathy. This case was recently discussed in detail elsewhere.21

Figure 4.

Figure 4.

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Panel A. Maximal intensity projection (MIP) image of whole-body 18FDG-PET demonstrates hypermetabolism in mediastinal lymph nodes (black arrows). Panel B. 18Fluorodeoxyglucose-PET/CT demonstrates hypermetabolism of spinal ganglia (white arrows) enabling the diagnosis of neurosarcoidosis (discussion of clinical details in Bartels et al, 2013).21 CT indicates computed tomography; PET, positron emission tomography.

Patient 5

A 53-year-old man reported difficulties in speaking by confusing words and sentences. As initially a stroke was assumed, the patient was admitted to the stroke unit. He was barely speaking and needed prodding to follow commands. The cerebrovascular workup was unremarkable. The diffusion-weighted MRI illustrated cortical hyperintense signal changes (Figure 5A) which were initially misinterpreted as ischemic areas. As the patient rapidly deteriorated, PET/CT scan was performed which showed a significantly diminished metabolism in the left hemisphere (Figure 5B). Together with the finding of EEG (continuous left-sided periodic sharp and slow wave complexes) and CSF findings (normal basic CSF results, measurement of protein 14-3-3 unfortunately failed due to small sample volume), sporadic Creutzfeldt-Jakob disease (CJD) was clinically diagnosed after consultation of the German prion research group in Göttingen. Some weeks later, the patient needed ongoing nursing home care and died 3 months after clinical diagnosis. An autopsy was not performed.

Figure 5.

Figure 5.

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Panel A. Cerebral MRI (diffusion-weighted sequence) shows cortical hyperintense signal changes in the left temporo-occipital region (white arrows). Panel B. 18Fluorodeoxyglucose-PET/CT shows hypometabolism (white arrows) in the left hemisphere affecting the frontal, parietal, temporal and occipital lobe. CT indicates computed tomography; MRI, magnetic resonance imaging; PET, positron emission tomography.

Reports on PET/CT findings in CJD are sparse. Mostly a nonvascular, asymmetric hypometabolism is encountered. Abnormal PET is detectable earlier than abnormal MRI and CCT findings.22 This is in accordance with our patient in whom PET/CT was much more pathologic than MRI and clearly excluded an ischemic lesion which can mimic early CJD.23,24

Patient 6

An 81-year-old woman was admitted due to acute right-sided hemiparesis. Magnetic resonance imaging showed multiple embolic ischemic lesions in both anterior and posterior circulation suggestive of cardioembolic origin (Figure 6A). Nine months earlier, a transcatheter aortic valve implantation (TAVI) was performed to relieve symptoms of aortic stenosis. Transoesophageal echocardiography showed no significant abnormalities. As the patient reported on additional general fatigue, weight loss, and pronounced sweating in the night, a whole-body PET/CT was performed to exclude unknown malignancy or systemic inflammation. Positron emission tomography/CT demonstrated hypermetabolism at the TAVI implant indicating an inflammatory process (Figure 6B). A following blood culture identified Streptococcus gallolyticus ssp pasteurianus and finally led to the diagnosis of TAVI endocarditis. A conservative treatment regimen with ampicillin/sulbactam over a period of 6 weeks resulted in sufficient recovery.

Figure 6.

Figure 6.

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Panel A. Cerebral MRI (diffusion-weighted sequence) shows multiple embolic ischemic lesions (white arrows) suggesting cardioembolic origin. Panel B. PET/CT shows hypermetabolism on the aortic valve after TAVI (white arrow). CT indicates computed tomography; MRI, magnetic resonance imaging; PET, positron emission tomography; TAVI, transcatheter aortic valve implantation.

Positron emission tomography for the diagnosis of infectious endocarditis in prosthetic valves and intracardiac devices has recently been advised.25 In our patient, there was no hint at TAVI endocarditis in transoesophageal echocardiography. However, by PET/CT during the further diagnostic work-up, TAVI endocarditis was found as the source of cardioembolic stroke.

Informed Consent

Informed consent was obtained from each patient.

Discussion

Cerebral PET scanning, isolated or combined with CT and recently with MRI, has become a unique success story in scientific research on neurophysiology and metabolism as well as on management of patients with neurologic disorders.1-4,8,26 However, limitations have to be considered, such as availability, timeliness, costs, logistical efforts, artefacts, and patients’ ability to cooperate.11,26,27 Thus, PET and its variants are rarely performed in acute neurological hospital care on admission as well as in the first days of hospitalization.

In all 6 presented cases, clinical and first imaging findings did not clarify sufficiently the underlying diseases. Positron emission tomography/CT was indicated in 5 cases to find or exclude a malignant tumorous process or a large vessel arteritis and in 1 case to differentiate an unclear thalamic lesion. In 1 case, PET/CT detected extracerebral disseminated hypermetabolism, leading finally to the diagnosis of sarcoidosis and neurosarcoidosis.21 In 2 cases, cerebral hypermetabolism was found, based on “luxury perfusion” and based on focal epileptic status, respectively. In 2 cases, hypometabolism was the distinctive finding: “empty zone” indicating abscess18 and severe hemispheric hypometabolism indicating CJD respectively. In 1 case, PET enabled the diagnosis of TAVI endocarditis as the cardioembolic source of multiple cerebral ischemic lesions. In Table 1, the additional diagnostic information gained by PET/CT is summarized.

Table 1.

Fluorodeoxyglucose-PET/CT Findings in 6 Acute Neurohospitalized Patients.

Patient Clinical Signs and Symptoms Imaging Results Before PET/CT Indication for PET/CT Additional Diagnostic Information of PET/CT Final Diagnosis
1 Acute hemiparesis, aphasic symptoms, B-symptoms MRI not possible, CCT masked by fogging effect Suspected malignancy and ischemic stroke Luxury perfusion indicating prior ischemic stroke Embolic stroke in the territory of anterior cerebral artery and partially middle cerebral artery
2 Rapid worsening of hemiparesis and somnolence By CCT and MRI thalamic lesion of unknown etiology Progressive cerebral process of unknown etiology Focal hypometabolism (empty zone) indicating abscess Thalamic abscess
3 Epilepsia partialis continua CCT and MRI not clarifying Possible paraneoplastic encephalitis, search for unknown malignancy or metastasis of previous breast cancer Ictal hypermetabolism in and anatomical delineation of the focal seizure zone Cryptogenic epilepsia partialis continua, exclusion of malignancy/paraneoplasia
4 Malaise, severe pain, bilateral facial palsy, spinal radiculopathy CCT and MRI not clarifying Possible paraneoplastic condition Hypermetabolism in mediastinal lymph nodes and spinal ganglia Sarcoidosis, neurosarcoidosis
5 Subacute severe aphasia, disorientation CCT unremarkable MRI suggesting stroke Progressive cerebral process of unknown etiology Hemispheric hypometabolism CJD
6 Acute hemiparesis, B-symptoms MRI demonstrated multiple ischemic lesions Search for a malignancy or systemic inflammation Hypermetabolism of aortic valve TAVI-endocarditis
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Abbreviations: CJD, Creutzfeldt-Jakob disease; MRI, magnetic resonance imaging; PET/CT, PET combined with computed tomography; TAVI, transcatheter aortic valve implantation.

Hitherto, 2 studies on a series of critically ill neurological patients investigated with PET or PET/CT have been reported.9,12 In the series of Kampe et al (2017), in 12 of 42 cases, direct therapeutic consequences could be deduced. In all their cases, as in ours, no adverse events related to transport and monitoring during the examination did occur.9 In another study, all of 10 cases with tick-borne encephalitis could be examined successfully with PET.12 Our patients have not been investigated prospectively in a protocol-based study, but according to clinical evaluation and after conventional diagnostic work-up. Nevertheless, the results of distinctive FDG-patterns in our patients enabled us to finalize it.

Reports on sensitivity and specificity of PET/CT are heterogeneous due to different indications such as nervous system disorders, malignancies, cardiovascular disease, and inflammation processes. Depending on the indication, the overall sensitivity is reported to be 70% to 90% whereas specificity is lower depending on the clinical problem and selection criteria.8 Considering the small case number of our report, we cannot calculate statistical parameters.

Although PET/CT could be performed safely in our patients, several limitations have to be discussed. First, the general interpretation of an abnormal PET/CT pattern is often challenging, especially if there is underlying comorbidity. In the presented cases, no severe concurrent cerebral diseases were present that would have biased the interpretation of PET/CT. However, in cases of a newly diagnosed disease in patients with concurrent known disease such as dementia, previous stroke and residual substance defect, interpretation may be difficult. Moreover, false-positive findings, for example diagnosis of brain metastasis instead of stroke or focal status epilepticus, have to be considered.28,29 Second, it has to be kept in mind that personnel, apparatus, and tracer costs are quite high. Third, not all patients are able to cooperate sufficiently during the at least 1-hour procedure in which they need to keep quiet and relaxed in a horizontal position. By pulse and oxygen-saturation monitoring and by administering slight sedation, if necessary, PET/CT acquisition can be completed in most cases. In the study of Kampe et al (2017), 15 of 42 patients were ventilated and 10 of 42 needed vasopressor support.9 Thus, combined with intensive care support, the colleagues could perform PET/CT successfully.9 However, availability and timeliness of the PET examination have to be ensured. Finally, radiation exposure may not be neglected. It is as low as 7 mSV in isolated PET and up to 25 mSV in PET/CT, depending on whether a low dose or a diagnostic CT is performed.21 In conclusion, MRI, CT, and ultrasound are still the most important imaging tools for the neurohospitalist in the diagnostic process and PET/CT plays a role as a supplementing imaging method. In selected cases, however, PET/CT provides a significant amount of information and hereby contributes essentially to find the correct diagnosis.

Acknowledgments

The authors thank H.P. Dinkel, MD, PhD, Head of the Department of Radiology, Municipal Hospital Landshut, Germany, for permission to demonstrate Figure 1B, 3A, 5A and 6A.

Footnotes

Author’s Contributions: J.G.H. conceptualized the paper, collected the data, and wrote the paper. W.N., M.B., and B.S. contributed to the evaluation and presentation of the PET/CT data and the discussion.

Declaration of Conflicting Interests: The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding: The authors received no financial support for the research, authorship, and/or publication of this article.

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