Links To And Excerpts From “The challenge of posterior circulation stroke (PCIS)” From EMC’s Episode 171 –

Note to myself: This podcast and show notes from Emergency Medicine Cases is outstanding. It is worth reviewing over and over.

I have simply copied and pasted this section’s show notes below because doing so helps me retain the material (spaced repetition).

In this post, I link to and excerpt from Emergency Medicine CasesThe challenge of posterior circulation stroke (PCIS) [0:00-27:00], from Ep 171 Posterior Stroke, EP Lead, HEAR Score, Ketamine for Suicidal Ideation, Peer Support Workers – Highlights from Calgary EM Hodsman Lecture Day.

Helman, A. Lang, E. Betzner, M. McRae, A. Lin, K. VandenBerg, S. Ross, M. Borgundvaag, B. Bradshaw, C. Posterior Stroke, EP Lead, HEAR Score, Ketamine for Suicidal Ideation, Peer Support Workers- Highlights from Calgary EM Hodsman Lecture Day. Emergency Medicine Cases. July, 2022. 7-6-2022.

All that follows is from the above resource.

fig1 when server ready

This is a special edition EM Cases main episode podcast. In April 2022, I was honoured to be the guest professor for Calgary EM at their annual Hodsman Lecture day.The day was essentially a series of live podcasts highlighting some of the amazing work they do, capped off by a lecture on compassionate care dedicated to the memory of Dr. Barbara Tatham. We covered a wide range of topics: The challenges of posterior strokes with Dr. Katie Lin; improving your ED flow by having an Emergency Physician Lead on shift with Dr. Eddy Lang and Dr. Michael Betzner; when not to order a troponin and the HEAR score (this is not a typo; this is not HEART Score) with Dr. Andrew McRae; ketamine for suicidal ideation with Dr. Marshall Ross; EM Peer Support Workers for patients with substance use disorder with Dr. Stephanie VandenBerg, plus a closely related bonus cast on SREMI’s incredible ED Pathway to Peers program for youth with mental health issues with Dr. Bjug Borgundvaag and Christine Bradshaw…

The challenges of posterior circulation stroke (PCIS)

Essential anatomy and corresponding deficits

Posterior circulation ischemic stroke (PCIS)/TIA involves the vertebrobasilar artery system (vertebral arteries arising from the subclavian arteries, three paired cerebellar arteries – AICA/PICA/SCA, the basilar artery, and the posterior cerebral arteries). Collectively, the posterior circulation supplies blood to the brainstem, cerebellum, occipital lobes, and thalami.

fig2 whenserv er ready

Cerebellar signs: vertigo, truncal/limb ataxia, nystagmus*

*truncal ataxia is evaluated by assessing the patient’s gait. If you can’t walk the patient, you can assess for truncal ataxia by asking the patient to sit up in the bed.

Brainstem signs: limb weakness, sensory loss, cranial nerve palsies, altered LOC

Occipital lobes: visual field deficits

The anatomic and functional complexity of the posterior circulation territory (esp. brainstem) make localization more challenging

Etiology of posterior circulation ischemic stroke (top 3)

Etiology differs from that of leading anterior circulation causes. In posterior circulation stroke, the most common causes are:

  1. Embolism (mostly cardiac eg. atrial fibrillation)
  2. Atherosclerosis (causing arterial stenosis)
  3. Arterial dissection (consider this etiology higher on the differential in younger patients who present with stroke symptoms)

Key point: the most common etiology of posterior circulation ischemic strokes is cardio-embolic, such as from atrial fibrillation

What are the key red flags to look for in the assessment for posterior circulation stroke? Think….”Dizziness + 1″

Red Flags to indicate possible PCIS: The “Dizziness +1” conditions

Isolated vertigo/ataxia/disequilibrium is very uncommon in PCIS, so look for accompanying “plus 1 red flags” to help trigger PCIS workup:

  • Presence of multiple vascular risk factors (older age, smoking, hypertension, hypercholesterolemia, diabetes, renal dysfunction, CAD/PVD, atrial fibrillation, structural cardiac conditions, previous MI/stroke)
  • Neck pain/recent head or neck trauma (dissection)
  • Severe occipital headache and/or altered LOC
  • Refractory nausea/vomiting (posterior fossa mass effect from ischemic edema)
  • Cranial nerve dysfunction:
    • “Dangerous D’s”: diplopia, dysarthria, dysphagia, dysphonia, dysdiadochokinesia*
    • Visual field deficit: occipital lobe
    • Acute hearing loss: pons
    • Unilateral limb ataxia: cerebellum (or associated cerebellar pathways)
  • Crossed face vs body symptoms (one side of face and opposite site of body – motor/sensory/ataxia domains)
  • Walk test patients to assess for truncal ataxia/dysequilibrium; often in stroke, the vertigo will be milder compared to peripheral causes but the disequilibrium and ataxia may be more severe

*Dysdiadochokinesia – StatPearls – NCBI Bookshelf:

“Dysdiadochokinesia (diadochokinesia) is the inability to perform rapid alternating muscle movements. These can be quick, synchronous, and can include pronation/supination, fast finger tapping, opening and closing of the fists, and foot tapping. It is an essential component to evaluate in patients suspected of having a cerebellar disease.”

Pearl: The vertigo in patients with a central cause tends to be less severe than that in peripheral causes of vertigo, while the ataxia in patients with a central cause of vertigo tends to be more severe than in patients with a peripheral cause.

Pitfall: While PCIS with isolated vertigo has been reported in the literature as a rare entity, it is incumbent upon the ED physician to perform a thorough history and physical looking for the “plus 1” features of PCIS. It may be that reported “isolated vertigo” is simply a reflection of poor history and physical exam assessments that have missed “plus 1” features, rather than truly isolated vertigo.

Walter Himmel’s detailed summary of his talk on approach to, and pitfalls/misconceptions in assessment of vertigo from EMU 2017

Locked in Syndrome – a unique presentation of posterior circulation ischemic stroke

Think about basilar stroke in patients who present with sudden collapse and persistent loss of consciousness with no clear alternative cause (ie. no signs of: significant head trauma, seizure, cardiac condition) – or “Locked in Syndrome“. Remember too that acute severe intracranial insult can be associated with hemodynamic instability and/or arrhythmias due to an overwhelming catecholamine surge. A key clinical clue to Locked in Syndrome from a basilar stroke is that the extra-ocular movements (EOMs) are spared, so be sure to open the patient’s eyelids and ask them to move their eyes; if they are able to move their eyes on command but lack all other motor function, consider Locked in Syndrome.

The locked in patient can’t open their eyes, but they can show extra-ocular movements when the examiner holds the patient’s eyes open and asks him/her to move the eyes.

Pearl: A key clinical clue to Locked in Syndrome from a basilar stroke is that the EOMs are spared, so be sure to open the patient’s eyelids and ask them to move their eyes; if they are able to move their eyes but lack all other motor function, consider Locked in Syndrome.

Which ED assessment components are most helpful for stroke decision-making in patients with posterior circulation ischemic strokes?

  • Ensure the patient is stable enough to go for imaging. PCIS patients are at higher risk for nausea/vomiting (ie. soiled airway) and decreased LOC (may need airway protection).
  • Remember PCIS-screening elements as part of your rapid neuro exam: facial droop, visual field deficit, eye movement abnormal/nystagmus, dysarthria (and other “Dangerous D’s”)*, gross motor/sensory screen, balance and limb ataxia (cerebellar symptoms)
    • *Dangerous D’s: Dizziness, Diplopia, Dysarthria, Dysphagia and Dysmetria
  • Check for potential contraindications to thrombolysis: Last seen normal time, acute trauma/bleeding, anticoagulant/antiplatelet medications, significant PMHx (ie. cancer, recent surgery)
  • Additional helpful data points: Goals of care and baseline functional status (ie. would this reasonably benefit from treatment?)

Suggested criteria are for calling a code stroke for the patient that you suspect has just suffered a posterior stroke

*Note that these criteria are location-specific and may be different than your local criteria.

  • Disabling deficits presenting <6h since time of onset if during waking hours OR
  • <24h of last seen normal if new symptoms upon awakening from sleep (ie. “wake-up” stroke).

Evidence suggests most “wake-up” cases occur within 1-2h of patient awakening, likely due to diurnal cortisol and BP spike as your body prepares to wake up, so true “wake-up” patients may often be within a tissue treatment window.

Acute posterior ischemic stroke treatment

See show notes for discussion of endovascular therapy and IV thrombolysis.

Bottom line for IV thrombolysis for posterior circulation ischemic stroke

IVT within 4.5h and in select “wake-up” stroke cases may improve functional outcomes based on preliminary data, and appears to be associated with slightly better outcomes and safety profile compared to anterior circulation ischemic stroke. This would be weighed carefully against risks, and generally would only be considered for disabling deficit cases with favourable imaging features (favourable imaging also carries a lower risk of hemorrhage after tPA).

This entry was posted in Emergency Medicine Cases, Neurology. Bookmark the permalink.