March 2019 By PsychDB.com

Approach to Neurologic Emergencies

Neurologic Emergencies must be managed efficiently and quickly, and several common presentations occur in the emergency setting.

A Stroke is any vascular injury that reduces cerebral blood flow to a specific region of the brain. A TIA (transient ischemic attack) is a brief episode of neurologic dysfunction caused by a focal disturbance of brain or retinal ischemia, with clinical symptoms typically lasting less than 1 hour, and without evidence of infarction.

Etiology
  • Ischemic (80%)
    • large vessel & small vessel (33%)
    • Cardioembolic (25%)
    • Uncommon mechanisms (e.g. - vertebral/carotid dissections, hypercoagulability)
    • Unknown etiology (>33%)
  • Hemorrhagic (10%)
  • Subarachnoid Hemorrhage (10%)

Differential Diagnosis: Bell's Palsy vs. Stroke

Approach to Stroke vs. Bell's Palsy

Anatomy

Circulation of the brain is provided through anterior and posterior circulation:

  1. Anterior circulation via the internal carotid arteries, anterior cerebral arteries (ACA), and middle cerebral artery (MCA) perfuses 80% of brain. This includes the optic nerve, retina, fronto-parietal and anterior-temporal lobes, and more
  2. Posterior circulation via the vertebral arteries, basilar artery, posterior cerebral artery, and posterior communicating artery perfuses the other 20% of the brain. This supplies the brainstem, cerebellum, thalamus, visual occipital cortex, and more

Localization

Stroke Localization

Stroke location Symptoms
ACA (anterior cerebral artery) stroke • Primarily frontal lobe function
• Paralysis/hypesthesia of lower limb on contralateral side
• Lower limb weakness > upper limb
• Impaired judgement/insight
MCA (middle cerebral artery) • Marked motor/sensory findings (upper limb > lower limb) on contralateral side
• Ipsilateral hemianopsia
• Agnosia common
• Aphasia common if dominant hemisphere affected
Posterior Circulation Stroke (vertebrobasilar) • Widest variety of symptoms, difficult to diagnose
• Cranial nerves, cerebellum, neurosensory tract involvement
• Vision and thought processing may be involved (occipital and parietal lobes)
• May have “crossed deficits” - bilateral findings
Differential Diagnosis
  • Epidural/subdural hematoma
  • Brain tumour/abscess
  • Air embolism
  • Metabolic (ie. hypo/hyperglycemia)
  • Wernickeʼs encephalopathy
  • Migraine
  • Seizure (Toddʼs paralysis)
  • Others

Investigations

  • If the acute stroke has been less than 4 hours, a Code Stroke should be activated for consideration for thrombolysis (tPA). The blood pressure must be < 185/110, and no other contraindications.
  • Immediate investigations
    • bedside glucose, unenhanced CT head, ECG
    • CT usually negative for 6-12 hours, but may show hyperdense artery sign (acute thrombus in vessel), sulcal effacement, loss of gray-white interface, loss of insular ribon, mass effect, acute hypodensity
  • Follow up investigations
    • CTA - useful to identify intravascular thrombosis, dissection, stenosis
    • MRI - evolving use, more sensitive for posterior circulation stroke and diagnosing early ischemic stroke
  • Other investigations
    • Echocardiogram
    • Carotid duplex scan
    • Angiogram
    • Additional bloodwork

Management

In acute ischemic stroke, hypertension should be managed and monitored. If using thrombolysis, one should treat to blood pressure < 185/110. If not a candidate for thromblysis, only treat if BP > 220/120, and aim for 10-20% reduction. Anti-hypertensives like nitrendipine, labetalol, nitroprusside can be used.

Altered LOC Etiologies

Differential
Metabolic/systemic derangements Delirium, hypoxia, DKA, hypoglycemia, hypoperfusion, infection, toxic drug effects, post-ictal states, electrolyte disturbance, glucose disturbance
Structural lesions Head trauma (SDH, EDH, SAH, concussion), stroke (thrombotic, embolic, hemorrhagic), tumour (mass effect, edema, bleeds), infection (meningitis, abscess, mass)
Etiology

Think about the context of the symptoms: the elderly are more susceptible to infectious etiologies, medication changes, stroke, occult trauma (e.g. - chronic SDH), young adults/adolescents are more susceptible to recreational drug use and trauma, and children are more susceptible to accidental toxic ingestions. Hypoactive delirium should be a diagnosis of exclusion and it is important to rule out any acute medical causes. Always check if the patient is protecting their airway (a VBG can be useful - if there is worsening hypercarbia, this requires an ICU consult!)

Physical Exam

  • Assess and reassess ABCs, GCS, focused neurological exam
  • Vital signs: hypotension, temperature abnormalities, Cushing response, respiratory rate
  • Pinprick glucose
  • Head to toe exam: pupillary reflexes, head trauma, mucous membranes, neck (meningismus, immobilize in trauma)
  • Check for gross blood, pus, retained FB on rectal/GU exam
  • Cutaneous - look for rashes/perfusion/needle tracks

Management

  • Review medications, hold any sedating medications
  • Ongoing ABCs and DEFG (donʼt ever forget glucose)
  • IVs, oxygen, and monitors
  • Consider using a “coma cocktail” of oxygen, naloxone, D50W, and thiamine
  • VBG if VBG to look for hypercapnia
  • If there are localizing signs, consider an urgent CT head
Presentation

The most common cause of Subarachnoid Hemorrhage (SAH) is trauma, and in non-traumatic cases, about 80% is due to aneurysms. SAH can present in one of three ways:

  1. Decreased LOC or Headache/focal signs
  2. Classic presentation (sudden/abrupt, intense severity 10/10 pain, unique quality not like typical headache they have had, associated symptoms of nausea/vomiting, syncope, seizures, diplopia
  3. Atypical presentation
    • Diagnostic challenge
    • Patient often looks well
    • SAH will be small volume and have a greater chance of negative head CT

Physical Exam

  • Examination is often unremarkable
  • Hypertension - important clue
  • Nuchal rigidity - 70% of cases
  • Cranial neuropathy, esp. CN III
  • Cranial nerve III palsy in 10-15% of SAH

Investigations

  • Unenhanced CT head
  • LP - look for RBCs (present in all SAH < 12 hours), xanthochromia (yellowish discolouration due to hemoglobin breakdown), and increase opening pressure (elevated in 66% of cases)

Management

If you witness a seizure, call for help, as the patient will likely have decreased LOC following the event. It is appropriate to call a code blue (“Medical Emergency”) if you need medications or more support. The first line treatment is with benzodiazepines either IV (preferred or IM). Give lorazepam 2mg, or midazolam 2mg, or diazepam 5mg q2-5minutes PRN until seizures are controlled. If not already on antiepileptics, it is reasonable to load them with dilantin (20mg/kg) to prevent further seizures.

Primer

Cauda Equina Syndrome is a neurological syndrome caused by compression of the nerve roots of the cauda equina. The most common cause is due to massive midline disk herniation. There is a classic triad of:

  1. Saddle anesthesia
  2. Loss of bowel/bladder function (overflow incontinence)
  3. Lower extremity weakness (at multiple spinal levels).

Physical Exam

  • Lower extremity weakness and numbness
  • Decreased DTRs
  • Saddle anesthesia
  • Decreased anal sphincter tone (up to 80%)
  • Positive SLR
  • Post void residual > 150cc (high sensitivity/specificity)

Investigations

  • Whole spine MRI is the gold standard
  • CT-myelography - invasive, less sensitive/specific
  • Plain films - generally not helpful