An elderly gentleman with a pmh of ulcerative proctitis on mesalamine and azathioprine, HTN, HLD, and DM2, who presented with cryptogenic stroke found to have a grade V aortic atheroma on TEE. He later presented with a venous sinus thrombosis – patient thought to potentially be hypercoagulable given history of ulcerative proctitis. .
Management of aortic atheromas from the American Heart Association/American Stroke Association-> for patients with an ischemic stroke or TIA and evidence of aortic arch atheroma, antiplatelet therapy is recommended (Class 1; Level of Evidence A); statin therapy is also recommended (Class 1; Level of Evidence B); the effective of anticoagulation with warfarin compared with antiplatelet therapy is unknown and surgical endarterectomy of aortic arch plaque for purposes of secondary stroke prevention is NOT recommended.
Mechanisms of cryptogenic stroke ->
1) cardiac embolism 2/2 paroxysmal atrial fibrillation, aortic atheromatous disease, or other cardiac sources
2) Paradoxical embolism
3) Undefined thrombophilia -> the patient in this case was worked up for thrombophilia!
4) Substenotic cerebrovascular disease (ie, intracranial and extracranial atherosclerotic disease causing less than 50% stenosis) and other vasculopathies (eg, dissection)
Workup of cryptogenic stroke -> the minimum workup for cryptogenic stroke includes:
-Noncontrast brain CT or brain MRI
-Serum electrolytes/renal function tests
-CBC including platelet count
-Markers of cardiac ischemia
Great link regarding workup of cryptogenic stroke:
A middle aged woman with a hx of severe bilateral glaucoma (legally blind), breast CA in remission who presented with acute proximal lower extremity weakness and subacute dysphagia admitted for statin-induced myositis due to elevated CK, eventually requiring intubation due to difficulty maintaining secretions, and found to have positive AQP4 Ab confirming the diagnosis of neuromyelitis optica.
- NMO is an inflammatory CNS disorder characterized by severe, immune-mediated demyelination and axonal damage mainly affecting the optic nerves, spinal cord, brain and brainstem. It is distinguished from MS by the presence of AQP4 antibody.
- Its incidence is 10 times higher in women than in men and more common in people of Asian, Hispanic, and African descent. Median age of onset is 32-41 years.
- Main clinical features include optic neuritis, acute transverse myelitis, area postrema syndrome.
- Evaluate with brain and spinal cord MRI, AQP4 Ab status, CSF analysis
- Diagnosis: Pt has at least one core clinical characteristic; enhancements on brain and spinal cord MRI; positive AQP4 IgG serum (and often CSF) autoantibody status; and exclusion of alternative diagnoses.
- Treatment: high dose IV methylprednisolone, plasma exchange, and immunosuppression treatment long-term disability and mortality rates are high
An elderly man with history of CKD 2/2 Wegner’s presents w/ hypothermia after being found down 2/2 presumed sepsis. He initially improved with warming and antibiotics, but about 24h into his course became completely unresponsive requiring intubation. No etiology was ever discovered for his altered mental status (including a w/u for meningitis, seizures, bleed) but he spontaneously woke up several days letter. It was ultimately thought that his mental status changes were most likely due to cefepime neurotoxicity, which often occurs in the setting of excessive antibiotic doses in patients with renal failure.
*What is cefepime neurotoxicity, and when should I consider it?
-Consider in a patient who came in with sepsis and develops new or worsening mental status after starting antibiotics
-Presents as encephalopathy, myoclonus, or seizures without another clear cause
-Occurs in patients with renal failure who receive excessive doses
-Associated with abnormal EEGs
See review here:
A elderly man with a pmh of diabetes, CKD, HTN, HLD and hx of splenic inf CAD with dilatation of his coronary arteries who presented with 2 days of severe, new onset headache and worsening vision changes. Initial CT demonstrated bilateral occipital hypodensities ? stroke. MRI confirmed ischemic stroke.
-DDx in this case was broad. The headache was highly suggestive of a non-ischemic etiology. Ischemic strokes normally do NOT present with headache. Additionally, the broad distribution of the findings on CT scan suggested the possibility of a vasculitic process.
-DDx included ischemic stroke, PRES, and vasculitis
-PRES typically presents with: headache, seizures, visual disturbances, and altered consciousness – this patient met 2/4 of these criteria
-Kozak’s rads tips –> Acute ischemic stroke on DWI MRI will appear as hyperintense “bright”. Ischemic stroke on ADC mapping ischemia will will be dark “hypointense”. PRES will have opposite imaging characteristics.
An elderly woman with MDS, PV, vascular disease presents with worsening vertigo lasting minutes to an hour. Given her comorbidities and initial inability to walk, we were concerned for central causes of vertigo; however, MRI (without contrast due to RF) was unchanged and the patient ultimately improved with PT and meclizine.
We discussed distinguishing peripheral vs central vertigo. While there is no perfect way to distinguish these two, typically the two differ in their timing, severity, and presence of auditory symptoms.
Central vertigo: Gradual, constant, not associated with auditory symptoms.
Thank you Ben for this awesome vertigo handout:
A note on gadolinium and risk of nephrogenic systemic fibrosis (NSF):
-For patients with a STABLE creatinine and GFR < 30, one should weigh risks and benefits before administering gad (our patient’s GFR was ~19, so definitely good to hold off if able!)
-Although there is no clear evidence that HD after gadolinium decreases risk of NSF, experts still recommend it if a patient is on HD and has eGFR < 15
Maneuvers for BPPV (see video in link):