MRI and CT appearances in metabolic encephalopathies due to systemic diseases in adults

Bathla, Girish; Hegde, Anaita Udwadia

doi:10.1016/j.crad.2012.05.021

Cited by 61 publications

(61 citation statements)

References 48 publications

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“…Furthermore, the MRI was only hours after the onset of SE, while the patient's ammonia level had been increasing over days, allowing for more opportunity to create such an abnormal MRI. The diffusion restriction was almost all cortical and symmetric; it spared the occipital lobes and, more importantly, the thalami and basal ganglia, which have only been involved in one case report of HE [2,10]. On the subsequent MRI, 4 days later, there was new CDR in the occipital lobes, thalami, and basal ganglia, while the original areas of CDR had progressed to cerebral edema.…”

Section: Resultsmentioning

confidence: 95%

“…Our case highlights that whenever extensive CDR is present, one should consider hypoxic and hypoglycemic insult first as they are common and characteristic of this pattern of injury but also consider HE and SE [2], which necessitate diagnostic tests that may not otherwise be performed. In this clinical setting, a serum ammonia level should be checked and trended over at least 2 days.…”

Section: Resultsmentioning

confidence: 99%

“…The most common areas of diffusion restriction are the insular cortex and cingulate gyrus, which are involved in almost all patients. It is rare to have involvement of the occipital cortices in HE, and involvement of the thalami and basal ganglia has only been reported in one patient [2,10]. In addition to cortical diffusion restriction there is often generalized cerebral edema, which can lead to death [9].…”

Section: Discussionmentioning

confidence: 99%

“…Diffusion restriction on MRI usually involves both brain cortex and subcortex, often corresponding to a vascular territory after ischemic stroke or a localized area around a lesion, but some disease processes result in diffusion restriction that is specific to the cortex, such as hypoxic brain injury and hypoglycemia [2]. Cortical diffusion restriction (CDR) has been well described in patients in nonconvulsive SE and also postictally after SE [3].…”

Section: Discussionmentioning

confidence: 99%

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Hyperammonemic Encephalopathy with Diffuse Cortical and Thalamic Signal Changes on Diffusion-Weighted Brain MRI

Yoon¹,

Choi²,

Kim³

2016

J Neurocrit Care

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Comorbid hyperammonemic encephalopathy (HE) and status epilepticus (SE) leading to extensive cortical diffusion restriction (CDR) on MRI have not been previously reported. We describe a patient with HE who subsequently developed provoked SE. Sequential MRIs demonstrated a progressive CDR that involved the entire bilateral supratentorial cortex, thalami, and basal ganglia, resulting in death from cerebral edema and brain herniation. Diffuse CDR is most frequently seen after hypotension or hypoxia, which our patient did not experience. Such findings have also been described in both HE and SE (Milligan et al. (2009), Chatzikonstantinou et al. (2011), U-King-Im et al. (2011), and Bindu et al. (2009), but not to the extent seen in our patient. Additionally, our patient had distinct radiologic features of both disease processes, suggesting a cumulative effect. The diagnosis of HE and SE in the setting of extensive CDR should not be missed and could lead to improved outcomes for two progressive, malignant, and treatable illnesses that can be easily overlooked. Case ReportWe present a 50-year-old female with cirrhosis secondary to chronic hepatitis C and alcohol abuse in remission who was admitted to our hospital with a three-day history of worsening abdominal pain and confusion. She was prescribed lactulose for the hepatic encephalopathy, which kept her ammonia in the normal range but had missed several doses over the preceding three days in addition to a decrease in the number of bowel movements. On initial exam the patient was normotensive and oxygenating well on room air with mild encephalopathy. A chronic ventral hernia displayed no signs of peritonitis. Labs on admission were significant for an ammonia level of 87 mol/L (18-72 mol/L), platelet level of 96 k/ L, sodium of 132 mmol/L, and international normalized ratio (INR) of 1.6. Computed tomography of her abdomen and pelvis with intravenous contrast revealed that the hernia contained dilated small bowel but no definitive obstruction.Overnight her mental status declined and by the next morning she was difficult to arouse and unable to follow commands. Vitals were within normal limits and morning labs were significant for a rise in plasma ammonia to 277 mol/L. She was electively intubated for airway protection but was not hypoxic. The following morning, on hospital day 3, she developed rhythmic clonic facial movements with eyelid fluttering, sustained tonic stiffening of the extremities, and intermittent right upper extremity jerks. The neurology service was consulted and continuous electroencephalogram (EEG) was recommended. During two hours of recording, prior to MRI imaging, there was focal status epilepticus in the left temporal region that spread to the left central and right temporal regions. 5 mg of intravenous lorazepam was administered and 1 gm levetiracetam twice daily was started, but the EEG continued to show persistent SE. She was paralyzed with vecuronium to obtain MRI of the brain with gadolinium contrast. This revealed extensive CDR involving the b...

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Section: Resultsmentioning

confidence: 95%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Hyperammonemic Encephalopathy with Diffuse Cortical and Thalamic Signal Changes on Diffusion-Weighted Brain MRI

Yoon¹,

Choi²,

Kim³

2016

J Neurocrit Care

View full text Add to dashboard Cite

show abstract

“…On MRI, involved regions appear as areas of fluid-attenuated inversion recovery hyperintense signal and T1 and T2 prolongation, which are not typically restricted on DWI. 62,68 The parietal and occipital lobes are most commonly affected, followed by the frontal lobes, the inferior temporal-occipital junction, and the cerebellum. 60,61,63 Basic PRES patterns resemble brain watershed zones with both the cortex and subcortical and deep white matter involved to varying degrees.…”

Section: Cavernous Sinus Thrombosismentioning

confidence: 99%

MRI in the Evaluation of Acute Visual Syndromes

Mukhi

Lincoln²

2015

Topics in Magnetic Resonance Imaging

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Acute visual symptom emergencies occur commonly and present a challenge to both clinical and radiologic facets. Although most patients with visual complaints routinely require clinical evaluation with direct ophthalmologic evaluation, imaging is rarely necessary. However, there are highly morbid conditions where the prompt recognition and management of an acute visual syndrome (AVS) requires an astute physician to probe further. Suspicious symptomatology including abrupt visual loss, diplopia, ophthalmoplegia, and proptosis/exophthalmos require further investigation with advanced imaging modalities such as magnetic resonance imaging and magnetic resonance angiography. This review will discuss a variety of AVSs including orbital apex syndrome, cavernous sinus thrombosis, cavernous carotid fistula, acute hypertensive encephalopathy (posterior reversible encephalopathy syndrome), optic neuritis, pituitary apoplexy including hemorrhage into an existing adenoma, and idiopathic intracranial hypertension. A discussion of each entity will focus on the clinical presentation, management and prognosis when necessary and finally, neuroimaging with emphasis on magnetic resonance imaging. The primary purpose of this review is to provide an organized approach to the differential diagnosis and typical imaging patterns for AVSs. We have provided a template for radiologists and specialists to assist in early intervention in order to decrease morbidity and provide value-based patient care through imaging.

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Neuroimaging for differential diagnosis of transient neurological attacks

Wang

Zha

2022

Brain and Behavior

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Background: Rapid yet comprehensive neuroimaging protocols are required for patients with suspected acute stroke. However, stroke mimics can account for approximately one in five clinically diagnosed acute ischemic strokes and the rate of thrombolyzed mimics can be as high as 17%. Therefore, to accurately determine the diagnosis and differentiate mimics from true transient ischemic attacks, acute ischemic stroke is a challenge to every clinician. Discussion: Medical history and neurological examination, noncontract head computed tomography, and routine magnetic resonance imaging play important roles in the assessment and management of patients with transient neurological attacks in the emergency department. This review attempts to summarize how neuroimaging can be utilized to help differentiate the most common mimics from transient ischemic attack and acute ischemic stroke. Conclusion: Although imaging can help direct critical triage decisions for intravenous thrombolysis or endovascular therapy, more detailed medical history and neurological examination are crucial for making a prompt and accurate diagnosis for transient neurological attack patients. K E Y W O R D S acute ischemic stroke, computed tomography, magnetic resonance image, transient and neurological attack, transient ischemic attack 1 INTRODUCTION Transient neurological attacks (TNAs) are common causes of emergency department (ED) visits. The final diagnosis of patients with TNAs can be divided into three categories: transient ischemic attack (TIA), acute ischemic stroke (AIS), and mimics (Mimics) after obtaining medical history, neurological examination, laboratory tests, and neuroimaging. As the risk of stroke recurrence or progression is highest in the 90 days following the first episode of either TIA or AIS, these two causes are of greatest concern. However, focal ischemia is not the cause of most TNAs. According to the literature, Mimics account for This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

show abstract

MRI and CT appearances in metabolic encephalopathies due to systemic diseases in adults

Cited by 61 publications

References 48 publications

Hyperammonemic Encephalopathy with Diffuse Cortical and Thalamic Signal Changes on Diffusion-Weighted Brain MRI

Hyperammonemic Encephalopathy with Diffuse Cortical and Thalamic Signal Changes on Diffusion-Weighted Brain MRI

MRI in the Evaluation of Acute Visual Syndromes

Neuroimaging for differential diagnosis of transient neurological attacks

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