Paroxysmal Sympathetic Hyperactivity Assessment Measure

Use CFS + DLT for diagnosis:

  • <8 = PSH unlikely
  • 8 to 16 = PSH possible
  • ≥17 = PSH probable

If total score 8 or greater, then use the CFS scale for monitoring of evolution (document daily maximal score).


Neurocritical Care Fellowship Learning Resources

Here’s a compilation of resources that I used during neurocritical care fellowship. Handy list of must-read books / articles / courses.


  • Zakaria, A. (2014). Neurocritical care board review. New York, NY: Demos Medical Publishing
  • Izzy, S., Lerner, D., & Lee, K. The NeuroICU Board Review
  • Levy, Z. (2017). Absolute Neurocritical Care Review. Cham: Springer International Publishing
  • Wijdicks, Eelco, et al.  Mayo Clinic Critical and Neurocritical Care Board Review.  OXFORD. Oxford University Press UK (2019)



  • Criner, G., Barnette, R., & D’Alonzo, G. (2010). Critical care study guide. New York: Springer
  • All SCCM Guidelines à SCCM | Guidelines. (2021). Retrieved 11 January 2021, from
  • Marino, Paul. The ICU Book 2014. Lippincott, Williams & Wilkins.


  • read landmark articles from NEJM, etc – thrombectomy trials, tPA trials, wake-up trials


  • Lee, K. (2018). The NeuroICU Book, 2e. New York, N.Y.: McGraw-Hill Education LLC
  • TBI –> Carney, N., Totten, A., O’Reilly, C., Ullman, J., Hawryluk, G., & Bell, M. et al. (2016). Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery, 80(1), 6-15. doi: 10.1227/neu.0000000000001432
  • NCS Website Guidelines à Neurocritical Care Society Guidelines. (2021). Retrieved 11 January 2021, from
cover image for: The neuroICU book


  • Tatum, W. Handbook of EEG interpretation


  • Le Roux, P. (2013). Monitoring in neurocritical care. Philadelphia: Saunders Elsevier
Cover of Monitoring in Neurocritical Care


  • Nadgir, R., Neuroradiology: The Requisites, Fourth Ed.  Elsevier, Inc
  • Applied Cerebral Angiography by Gianni Bradac


  • Greenberg, M. Handbook of neurosurgery 9th Ed.  Thieme



  • ESETT = Established Status Epilepticus Treatment Trial
    • Randomized, blinded, adaptive trial
  • GOAL: compare efficacy of 3 intravenous AEDs in children and adults with convulsive status epilepticus unresponsive to treatment with benzos.
    • Levetiracetam
    • Fosphenytoin
    • Valproate
    • Primary outcome:
      • absence of clinical seizures + level of consciousness at 60 mins
    • Safety outcomes:
      • life-threatening hypotension
      • cardiac arrhythmia
      • intubation
      • seizure recurrence
      • death
    • 384 patients
    • Primary outcome of cessation of status epilepticus
      • levetiracetam 47%
      • fosphenytoin 45%
      • valproate 46%
    • Safety outcomes
      • more episodes of hypotension and intubation with fosphenytoin (not significant)
      • more deaths in levetiracetam (not significant)
    • time to cessation of seizures favored valproate but not subjected to formal analsyis
    • Each of the three seizure meds led to cessation of status epilepticus and improved alertness by 60 mins in ~half of patients, with similar incidences of adverse events.


  1. Eligibility: 2 years or older, treated with generally accepted cumulative dose of benzos lasting >5mins and with persistent or recurrent convulsions at least 5 mins after last dose of benzos and no more than 30 mins after last dose of benzos
  2. “Minimal adequate cumulative dose” defined in the study as:
    1. diazepam at 10mg (IV or per rectum)
    2. lorazepam at 4mg (IV)
    3. midazolam at 10mg (IV or IM)
  3. After 10 mins, infusion of trial drug discontinued; rescue therapy given as needed for persistent or recurrent seizures after 20 mins from start of drug infusion.
  4. “clinically apparent seizure” defined as visually observed focal or generalized tonic-clonic movements or generalized or segmental myoclonus.
  5. “improved responsiveness” defined as purposeful responses to noxious stimuli, ability to follow commands, verbalization
  6. Planned interim analysis (at n=400) met predefined futility criterion, and trial was stopped.


  1. need for unblinding in some instances
  2. 10% of patients had psychogenic nonepileptic seizures
  3. clinical rather than EEG criteria was used to determine primary outcome
  4. fosphenytoin restrictions on maximal rate of infusion, so constraint of 10-minute infusion limited maximal dose to 1500mg PE which may be submaximal dose
  5. adverse events >24h not collected – may have missed other events such as rashes or elevated liver enzymes or delayed presentations
  6. high percentage of patients had deviations related to benzodiazepine dosing

TAKE HOME: Fosphenytoin, valproate, and levetiracetam are effective in approximately half of patients with benzo-refractory status epilepticus. These 3 intravenous meds did not differ significantly with regard to effectiveness and safety.


Brown, J., & Jones, J. (2020). Randomized Trial of Three Anticonvulsant Medications for Status Epilepticus. The Journal Of Emergency Medicine58(6), 980-981. doi: 10.1016/j.jemermed.2020.05.027

LHH ERAS Protocol for Spine Surgery

Pre-hospital phase (to be done by surgeon)

    • Encourage smoking cessation x 1 month preop (consider concierge referral for smoking/tobacco cessation at Northwell Health)
    • BMI assessment
      • Discuss risks of obesity for BMI > 35
      • Consider referral to Bariatrics or to concierge Northwell Nutrition
  • LABS:
    • Glucose control
      • Check preop HgbA1C in diabetic patients
      • If HgBA1C >8 –> defer elective surgery or require endocrine optimization
    • Nutrition assessment: check albumin; assess for malnutrition low albumin
    • Assess Hct: if < 33 consider hematology consultation
    • Pain management consultation pre-op if chronic use of narcotics; arrange appropriate pre-opioid weaning if necessary
    • Consider allergy testing for PCN allergic patients if concern for anaphylaxis; test dose of cefazolin by anesthesia if patient states penicillin allergic
  • Arrange home and social support: Identify a home coach

Preop hydration:

  • No solid food on day of surgery
  • Clear liquids permitted until 3 hours before surgery
    • Nondiabetic: Carbohydrate loaded drink (Gatorade/Powerade) on way to hospital
    • Diabetic: 20 ounces of water 3-4 hours before surgery
  • NPO 3 hours prior to surgery
  • If in preop area >3 hours until surgery start time, can give Ensure Clear (8 ounces) in preop area (only if cleared by attending surgeon)
  • *If patient drinks anything other than clear liquids in the 8 hours prior to surgery, or drink clear liquids after 2 hours before surgery start time (other than a small sip with meds) the procedure will be postponed or cancelled

Preop medication (in holding):

  • Acetaminophen 1000mg PO (unless h/o liver disease or abnormal LFTs)
  • Aprepitant (Emend) 40mg PO
  • Gabapentin 300mg PO (hold if >70 y/o)
  • Celecoxib 200mg PO (optional)
  • *Patients on narcotics and gabapentin should take their home dose in AM of surgery


  • Dexamethasone 4-10mg IV pre-incision
  • Local Analgesia:
    • Lidocaine 1% before incision
    • Liposomal bupivacaine (Exparel) 20mg mixed with 20cc of 0.25% Marcaine (10cc of Marcaine if small incision) for local field block
    • Option for TLIP block by anesthesia instead of local field block
  • Fluid management
    • Maintain euvolemia throughout perioperative period
    • Prefer LR at 1-3 mL/Kg or another crystalloid
    • Replace fluid deficit (NPO, blood loss, urine, insensible) at discretion of anesthesiologist
  • Opioids:
    • Goal: minimize opiod use intraoperatively
    • Use of remifentanil with discretion by the anesthesiologist due to possible association with postop hyperalgesia
    • Titrate long acting opioids near end of case


  • Medications: (if patient admitted)
    • Acetaminophen 1000mg q8h PO standing (IV if cannot take PO)
    • Methocarbamol (Robaxin) 500mg q8h standing
    • Pregabalin (Lyrica) 50mg TID po standing (hold if > 70 yrs old)
    • Oxycodone 5mg po PRN for severe pain (PAS of 7-10)
    • Ondansetron (Zofran) 4mg sublingual q6h standing
    • Metoclopramide (Reglan) 10mg IV or po q8h PRN nausea/vomiting (second line)
    • *Dexamethasone (Decadron) 4mg q6h IV x 6 doses standing (hold if diabetic) (optional)
  • Physical therapy/Occupational therapy
    • Start PT in PACU if appropriate
      • Elevate HOB 10 degrees q10 min as tolerated x 3 (up to 30 degrees)
      • Dangle with assistance from RN
      • If lightheaded, increase IVF before PT
      • Out of bed and ambulating within 4 hours of arrival to PACU
    • Start PT and OT on POD #1
  • Early nutrition
    • Clear liquids PACU tray (encourage liquids, withhold if nauseated, bloated, or somnolent)
      • 1 Ensure clear or Enlive
      • 1 lemon ice
      • 2 cups of hot water to make tea or broth
      • Caffeinated coffee (if requested)
    • Regular diet ordered (unless airway concerns)
  • Early removal of catheters / drains
    • Remove Foley catheter on AM of POD #1 for inpatients
    • Avoid Foley catheter use in OR for short procedures (or remove at end of case)

Discharge Medications

  • Acetaminophen (Tylenol) 500mg PO standing q8h x 1 week
  • Oxycodone/acetaminophen (Percocet) 5/325mg PO q6h PRN for severe pain
  • Methocarbamol (Robaxin) 500mg po q8h PRN muscle spasm
  • Pregabalin (Lyrica) 50mg TID x 1 month
  • *Gabapentin 300mg BID if unable to get pregabalin


  • Department of Neurosurgery, LHH


Study published in Journal of Stroke and Cerebrovascular Diseases published Nov 2020 looking at the link between blood pressure and outcome in ICH patients using the data from the VISTA trials (Virtual International Stroke Trials Archive)

Retrospective analysis of VISTA-ICH trial. n=384. Results below.

 Odds of unfavorable outcome for blood pressure categories. Left: unadjusted ORs. Right: adjusted ORs.

Study concluded that elevated BP after ICH is associated with poor outcome and supports the practice of targeting SBP of 140 mm Hg.

Limitations of the study:

  1. observational nature
  2. small sample size
  3. study population skewed towards less disease severity

Note that ENLS (published 2017) changed guidelines:

…it may be reasonable to target a systolic blood pressure between 140 and 180 mmHg with the specific threshold determined based on patient comorbidities and level of chronic hypertension.

While AHA/ASA (published 2015) guidelines originally stated that: (prior to recent ICH trials being published)

For ICH patients presenting with SBP between 150 and 220 mmHg and without contraindication to acute BP treatment, acute lowering of SBP to 140 mmHg is safe (Class I; Level of Evidence A) and can be effective for improving functional outcome


Claude Hemphill, J., & Lam, A. (2017). Emergency Neurological Life Support: Intracerebral Hemorrhage. Neurocritical Care27(S1), 89-101. doi: 10.1007/s12028-017-0453-0

Francoeur, C., & Mayer, S. (2020). Acute Blood Pressure and Outcome After Intracerebral Hemorrhage: The VISTA-ICH Cohort. Journal Of Stroke And Cerebrovascular Diseases30(1), 105456. doi: 10.1016/j.jstrokecerebrovasdis.2020.105456

Hemphill, J., Greenberg, S., Anderson, C., Becker, K., Bendok, B., & Cushman, M. et al. (2015). Guidelines for the Management of Spontaneous Intracerebral Hemorrhage. Stroke46(7), 2032-2060. doi: 10.1161/str.0000000000000069

IV Diclofenac Sodium for Central Fever


  • initial bolus: 0.2 mg/kg in 100 ml of saline solution over 30 minutes
  • continuous infusion:
    • 75 mg in 50 ml NS
    • dosage 0.004–0.08mg/kg/hour titrated to body temperature
    • discontinued if temperature <37.5°C for more than 12 hours on a dose of 0.004 mg/kg/hour
  • Monitor BP, CBC, liver and kidney function
  • continuous monitoring of temperature with esophageal probe

Side effects: hypotension, reduced MAP. oliguria, reduced HR, CPP, PBtO2

Table. Studies on use of diclofenac in the ICU

Diclofenac sodium low dose IV infusion is not commonly used in the ICU for the treatment of central fever. Needs further studies and clinical experience. This method / dosing schedule is lifted from a case report on the successful treatment of central fever in a stroke patient. (reference below)


Giaccari, L., Pace, M., Passavanti, M., Sansone, P., Esposito, V., Aurilio, C., & Pota, V. (2019). Continuous intravenous low-dose diclofenac sodium to control a central fever after ischemic stroke in the intensive care unit: a case report and review of the literature. Journal Of Medical Case Reports13(1). doi: 10.1186/s13256-019-2281-7

Hemorrhagic Transformation in Stroke – Predictive Scores

Published predictive scores of hemorrhagic transformations

  • HTI: Hemorrhagic Transformation Index Score
  • ASPECTS: Alberta Stroke Program Early CT Score
  • iScore: Ischemic Stroke Predictive Risk Score
  • HAT: hemorrhage after thrombolysis
  • HeRS: Hemorrhage Risk Stratification Score
  • SEDAN: Blood Sugar [glucose] on admission, Early infarct signs and [hyper] Dense cerebral artery sign on admission computed tomography [CT] head scan, Age, and NIHSS
  • SITS- SICH: Safe Implementation of Treatments in Stroke (SITS) Symptomatic Intracerebral Hemorrhage Risk Score
  • GRASPS: Get With The Guidelines–Stroke symptomatic intracerebral hemorrhage risk
  • MSS: Multicenter rt-PA Stroke Survey Group Score
  • SPAN-100: Stroke Prognostication using Age and NIH Stroke Scale

Summary of predictors of hemorrhagic transformation.


ANDRADE, J., MOHR, J., LIMA, F., BARROS, L., NEPOMUCENO, C., PORTELA, L., & SILVA, G. (2020). Predictors of hemorrhagic transformation after acute ischemic stroke based on the experts’ opinion. Arquivos De Neuro-Psiquiatria78(7), 390-396. doi: 10.1590/0004-282×20200008

Brain-Heart-Lung Connection in SAH

How the brain, heart and lungs are connected in SAH.

Pathophysiology of cardiopulmonary complications in SAH. SAH leads to catecholamine surge, which activates alpha, alpha + beta, and beta receptors. This leads to pulmonary and myocardial dysfunction as well as platelet aggregation. Patients then develop neurogenic pulmonary edema, LV dysfunction and shock.


Muehlschlegel, S. (2018). Subarachnoid Hemorrhage. CONTINUUM: Lifelong Learning In Neurology24(6), 1623-1657. doi: 10.1212/con.0000000000000679

Pathophysiology of Delayed Cerebral Ischemia (DCI)

Historically, DCI thought to be caused by cerebral vasospasm. Recent studies now indicates DCI may be caused by several factors, including early brain injury, microthrombosis, cortical spreading depolarizations and related ischemia, in addition to cerebral vasospasm.

Cerebral vasospasm may be an epiphenomenon, and underlying biochemical and biophysical changes that lead to DCI occur as early as SAH onset.

Supporting evidence? Endothelin 1 is strongest vasoconstrictor mediator in SAH. Administration of clazosentan (potent endothelin 1 receptor inhibitor) resulted in less angiographic vasospasm but did not decrease DCI nor lead to improvement in 90-day outcomes.


Muehlschlegel, S. (2018). Subarachnoid Hemorrhage. CONTINUUM: Lifelong Learning In Neurology24(6), 1623-1657. doi: 10.1212/con.0000000000000679