ISCHEMIC STROKE

Poststroke recrudescence

David Goldemund M.D.
Updated on 25/10/2024, published on 24/10/2024
  • poststroke recrudescence (PSR) is an underrecognized clinical entity defined as a temporary recurrence or worsening of previous stroke-related neurological deficits
    • some other names can be found in the literature: re-emergence, exacerbation of focal neurological deficits, locus minoris resistentiae, metabolic insult causing reexpression of an old stroke
    • it belongs to a large group of stroke mimics
  • unlike recurrent strokes, recrudescence is not due to new ischemic events but results from physiological or external triggers
  • understanding the nature of PSR is essential, as misinterpretation may lead to unnecessary interventions
  • prognosis is typically favorable
  • research efforts should focus on developing validated predictive scores to identify patients at risk of PSR

Pathophysiology

  • poststroke recrudescence is thought to result from disturbances in the neural networks that were previously affected by stroke; minimal impairment of the remaining functioning neurons may produce an exaggerated response
  • the exact mechanisms remain unclear, but it is hypothesized that residual deficits from the original stroke are reactivated by physiological stressors rather than by new infarction or hemorrhage
  • contributing factors include:
    • infection – systemic infections, such as pneumonia, are common triggers
    • electrolyte and glucose imbalances (low sodium, potassium, or glucose levels)
    • fever 
    • medication and its changes – abrupt changes in medications, particularly those affecting blood pressure or anti-seizure therapy, benzodiazepines, or opioids
    • hypotension
    • excessive physical stress, fatigue, and lack of sleep

Clinical Presentation

  • PSR is characterized by transient worsening of residual neurologic deficits or transient recurrence of previous stroke-related focal neurologic deficits
  • patients with PSR typically have a history of similar episodes  (Sagiraju, 2023)
  • the deficit resolves after treatment of the precipitating factor, usually within hours to days

Diagnostic criteria of PSR (Topcuoglu, 2017)

  • transient (repeated) worsening of residual post-stroke focal neurologic deficits or transient recurrence of previous stroke-related focal neurologic deficits
  • identifiable trigger
  • chronic stroke on brain imaging + negative DWI
  • an unlikely alternative diagnosis
    • no clinical or EEG evidence of seizure around the time of the event
    • no suspicion for low-flow TIA from cerebral artery stenosis or occlusion

Diagnostic evaluation

Appropriate diagnosis of PSR is critical to avoid unnecessary evaluation for recurrent stroke and potentially harmful escalation of medical therapy for stroke prevention

  • a thorough history, clinical, and neurological examination
    • document previous stroke symptoms and compare them with current presentation
    • search for previous PSR attacks
    • compare actual signs with the last examination
    • inquire about recent infections, metabolic issues, or medication changes
  • perform immediate MRI with DWI to exclude new ischemic lesion (CT scan if MRI is unavailable or contraindicated)
    • chronic stroke findings on MRI:
      • lesion is hypointense on T1-weighted images and hyperintense on T2/FLAIR sequences
      • negative DWI
      • atrophy + cystic changes
  • laboratory testing – exclude the above-mentioned metabolic and infectious triggers
    • complete blood count, electrolytes, glucose levels
    • inflammatory markers (e.g., ESR, CRP)
    • coagulation profile
  • monitor vital signs (temperature, blood pressure, ECG, and oxygen saturation)
  • additional tests include EEG, TTE, vascular imaging (US, CT/MR angiography), etc.

Differential diagnosis

  • recurrent stroke or transient ischemic attack (TIA) 
    • PSR symptoms are identical to the previous stroke
    • new ischemic events often present with additional or evolving neurological signs
    • distinguishing TIA or crescendo TIA may be challenging in some cases
  • post-stroke seizures – seizures can mimic recrudescence but typically present with focal motor activity or altered consciousness
  • delirium or encephalopathy – infections and metabolic derangements lead to generalized cognitive decline rather than focal neurological deficits, aiding in differentiation

Management

  • thrombolysis issues
    • intravenous thrombolysis is well-tolerated in the stroke-mimic population  (Ali-Ahmed 2019)
    • PSR considerations should not lead physicians to withhold thrombolysis in acute cases where there is diagnostic uncertainty in otherwise eligible patients
  • identify and treat triggering factors (e.g., antibiotics for bacterial infection) can help alleviate recrudescence
  • manage the patient’s vascular risk factors and comorbid conditions
  • regular follow-up and patient education regarding early recognition of PSR and its triggers can further reduce the frequency of episodes
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Poststroke recrudescence
link: https://www.stroke-manual.com/poststroke-recrudescence/