Transient worsening of poststroke neurologic deficits or reemergence of previous stroke-related deficits (or poststroke recrudescence [PSR]) in the setting of toxic metabolic factors is a frequently encountered phenomenon
PSR is often referred to as an anamnestic recall or recrudescence and have associated it with systemic infections and the use of sedative medications and anesthetic drugs.
PSR can occur after ischemic and hemorrhagic stroke. Infection, hypotension, hyponatremia, insomnia or stress, and benzodiazepine use are important triggers. New neurologic deficits are usually mild to moderate in severity and do not exceed the previous stroke deficits.
Symptoms can start abruptly but can be remedied completely within hours or days after the resolution of the trigger (eg, treatment of an underlying infection). Climb deeper into this topic here ncbi.nlm.nih.gov/pmc/articles/P…@CPSolvers#VMR
The predominant face, arm, and leg involvement combined with the infrequent altered consciousness, gaze paresis, hemianopia, and extinction or inattention suggests that the long white matter tracts are more susceptible.
The association of PSR with insomnia and benzodiazepine use in our study and others implicates neurotransmitter systems pertaining to γ-aminobutyric acid.
Similar mechanisms have been implicated in other neurologic conditions associated with transient exacerbations, such as multiple sclerosis (Uhthoff phenomenon), migraine, and brain tumor.
• • •
Missing some Tweet in this thread? You can try to
force a refresh
Hematogenous dissemination then can occur typically 4 to 10 weeks later, giving rise to secondary syphilis. <40% of pts w/ syphilis have primary syphilis diagnosed. These “Secondary” lesions last for several weeks before spontaneously resolving. Coined “early, latent infection”
What does late infection mean? When syphilitic lesions recur after 1 year from the initial eruption, or seropositivity is detected more than 1 year after the initial eruption, it is termed late latent syphilis.
Some optics neuritis pearls in a short #Medtweetorial 🧵…. We all know that optic neuritis is frequently associated with multiple sclerosis (MS). But optic nerve inflammation can exist from autoimmunity, infection, granulomatous disease, paraneoplastic disorders, & demyelination
Classical ON from MS is unilateral, moderate, painful color vision loss with an afferent pupillary defect & normal fundus examination.
In those with ON, 95% of patients showed unilateral vision loss & 92% had associated retroorbital pain that frequently worsened w/ eye movement.
If you have not listened to the @CuriousClinPod most recent podcast (Episode 10: Why does metronidazole treat both bacterial and parasitic infections?) then I suggest you tune in.
I'll summarize their show notes here in short #medtweetorial
First a question:
Was metronidazole first used as an antibiotic or as an antiparasitic?
If you guessed antiparasitic, then you would be correct!
It was developed in the 1950s to treat the parasite trichomonas & then was used in the 1960s to treat other parasitic infections, like giardia and amoebiasis.
A 31-year-old M born and raised in Brazil w/ no PMH presented with a 3 mon history of worsening DOE, orthopnea, 7kg weight loss, abdominal distention, dry cough, and syncope
An interesting fact from @3owllearning : Depending on the clinical problems, the studies of disease probability for differential diagnosis often show 10 - 25% of cases are unexplained, even after careful examination and testing.