Case Presentation: Pachymeningeal enhancement (PME) is a radiological phenomenon describing the enhancement of the dura and outer layer of the arachnoid meninges best appreciated on contrast-enhanced MRI. We present a case of diffuse PME in the setting of a transient ischemic attack (TIA) which has been previously unreported. An 83-year old female with a history of rheumatoid arthritis presented with a three hour history of word-finding difficulties and right-sided weakness. Physical examination revealed 4/5 power in right lower extremity. Blood tests showed glucose 111mg/dL, INR 3.4 and ESR 6mm. CT head showed extensive chronic white matter gliosis. CT perfusion study, CTA head and neck were unremarkable. Non-contrast MRI brain revealed extensive dural thickening surrounding the posterior cerebral hemispheres and bilateral tentorium cerebelli. Neurological deficits improved albeit right lower extremity weakness persisted raising concern for cortical irritation. Contrast MRI brain showed smooth, thick, diffuse supra- and infratentorial PME extending through the foramen magnum without diffusion restriction. Neurological deficits resolved and she was discharged on dual antiplatelets. Outpatient lumbar puncture was normal including flow cytometry, cytology, ACE, cultures including AFB, VDRL and IgG4. Repeat contrast MRI brain demonstrated spontaneous complete resolution of dural enhancement.
Discussion: PME can occur in a thin discontinuous, thick continuous focal or diffuse pattern. The former is an incidental finding in ~50% of the population whereas the latter is indicative of intracranial pathology. Diffuse PME is most often attributed to spontaneous intracranial hypotension (SIH) wherein patients report postural headaches with rapid relief on recumbency. Classically, a smooth wave-like pattern is observed in the temporal and frontal lobes. Other differentials are far more ominous. Infectious causes include meningitis and tuberculosis typically present with leptomeningeal enhancement. Neoplastic conditions present with focal patterns whereas autoimmune conditions including neurosarcoidosis, IgG4 vasculitis and rheumatoid meningitis cause diffuse PME sparing the convexities of the cerebral hemispheres. Ischemic events resulting in PME are unreported. Interestingly, several studies have identified atypical presentations of meningitis with transient neurological dysfunction without nuchal rigidity mimicking TIAs. Cuinat et.al performed a retrospective study evaluating the frequency of meningeal disease amongst patients in a TIA clinic. In 529 patients, 134 patients were classified into non-ischemic events of which 9 patients were re-diagnosed with meningeal disease.
Conclusions: Our patient presented with transient neurological deficits with evidence of thick diffuse supra- and infratentorial PME on MRI. Despite a history of rheumatoid arthritis the pattern of enhancement was inconsistent and rheumatoid meningitis seldom occurs in severe flare-ups. SIH causes thin PME and our patient denied a history of headaches. Infectious meningeal etiology is unlikely as her condition improved without antimicrobial therapy. TIA causing PME is unreported and our patient had spontaneous clinical and radiological resolution thus excluding alternative causes of diffuse PME. Our case highlights the paramount importance and the diagnostic value of MRI in the evaluation of patients presenting with transient neurological dysfunction as misdiagnosis may be life-threatening.
