SummaryToxic leukoencephalopathy results from damage to the white matter caused by various toxins. It manifests itself as white matter signal abnormalities with or without the presence of restricted diffusion. These changes are often reversible if the insulting agent is removed early, with the exception of posthypoxic leukoencephalopathy that can manifest itself 1–2 weeks after the initial insult. However, many other potential causes of white matter signal abnormalities can mimic the changes of toxic leukoencephalopathy. Thus, familiarity with the causes, clinical presentation and particularly imaging findings of toxic leukoencephalopathy is critical for early treatment and improved prognosis. The purpose of this pictorial essay is to familiarize the reader with the various causes of toxic leukoencephalopathy along with its differential diagnoses and mimics.
Computed tomography (CT) and magnetic resonance imaging (MRI) have made it relatively easy to diagnose cortical convexity subarachnoid hemorrhages (cSAH); however, the evaluation of these hemorrhages should not be limited to size and location. It is imperative that possible underlying etiologies be identified so that clinicians may properly treat and prevent this potentially catastrophic event. The goal of this article is to review etiologies of cortical convexity subarachnoid hemorrhages, from common causes such as cerebral amyloid angiopathy to less common causes such as reversible cerebral vasoconstriction syndrome and moyamoya. The specific imaging findings of each etiology that may be responsible for these hemorrhages are described in this article so that the radiologist may properly aid in the diagnosis of the underlying cause.
Background:
Epidural hematomas are common intracranial pathologies secondary to traumatic brain injuries and are associated with overlying skull fractures up to 85% of the time. Although many require immediate surgical evacuation, some are observed for stability and followed up conservatively with serial imaging or enlarge slowly overtime, similar to chronic subdural hematomas. Those in the latter category may present with vague symptoms such as diplopia or headache and are often found on routine outpatient evaluation. When concerning findings such as significant mass effect are present, surgical evacuation is necessary.
Case Description:
Here, we present the case of a 32-year-old man who presented with diplopia 6 weeks after experiencing head trauma and was found to have a chronic epidural hematoma. On resection, thick, inflammatory tissue was observed and carefully resected, revealing normal dura underneath. Six weeks after evacuation of the hematoma, the patient had near-complete resolution of his diplopia and complete resolution of his epidural hematoma.
Conclusion:
Given the consistency and nature of the fibrous material observed intraoperatively in this case, near-complete resection of the tissue was likely necessary to help facilitate adequate reexpansion of brain parenchyma and improve clinical outcomes.
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