Posterior Circulation, Brainstem, and Cerebellar Syndromes

The subtle stroke problem

The posterior circulation supplies the brainstem, cerebellum, occipital lobes, thalami, and inferomedial temporal lobes. These strokes are heavily tested because they are easy to under-triage: a patient may say only "dizzy" when the real problem is diplopia, dysarthria, dysphagia, truncal ataxia, or evolving brainstem ischemia. Standard face-arm-speech screens miss many posterior events, which is why the BE-FAST mnemonic adds Balance and Eyes to Face, Arm, Speech, Time. The SCRN candidate should listen for posterior clues and then decide what could harm the patient in the next hour.

Posterior circulation syndrome map

Crossed brainstem syndromes

The defining brainstem clue is the crossed sign: an ipsilateral cranial nerve deficit paired with contralateral body weakness or sensory loss, because cranial nerve nuclei sit in the brainstem while the long motor and sensory tracts have not yet decussated. Three classic named syndromes appear on the exam:

• Lateral medullary (Wallenberg) syndrome from posterior inferior cerebellar artery (PICA) or vertebral occlusion: ipsilateral facial pain/temperature loss with contralateral body pain/temperature loss, dysphagia and hoarseness (CN IX/X), vertigo, nystagmus, ipsilateral limb ataxia, and ipsilateral Horner syndrome (ptosis, miosis, anhidrosis). There is typically no major limb weakness, but dysphagia and aspiration risk are high.
• Weber syndrome (midbrain, often PCA branch): ipsilateral CN III (oculomotor) palsy with contralateral hemiparesis.
• Millard-Gubler syndrome (ventral pons): ipsilateral CN VII (facial) palsy and often CN VI with contralateral hemiparesis.

Basilar occlusion and locked-in syndrome

Basilar artery occlusion is a neurologic emergency. Because the basilar feeds the pons and reticular activating system, occlusion can cause fluctuating or decreasing consciousness, quadriparesis, and locked-in syndrome, in which the patient is awake and aware but can move only the eyes vertically or blink.

A patient who seems unresponsive may actually be aware, so the nurse should speak normally, explain care, establish a yes/no eye-movement communication system, and test for vertical eye movement and blink-to-command rather than assuming the patient cannot perceive the environment. Pinpoint pupils, crossed signs, sudden coma, or rapidly fluctuating deficits should trigger immediate escalation for emergent imaging and possible thrombectomy.

A crucial testing caveat is that the NIHSS underweights posterior strokes. The scale was built around anterior (carotid) territory deficits, so a patient with a devastating brainstem or cerebellar event can score deceptively low because the scale captures little for vertigo, ataxia, diplopia, or dysphagia. A low NIHSS in a patient with crossed signs, sudden severe imbalance, or new bulbar symptoms should never reassure the nurse; the clinical pattern, not the number, drives escalation. This is why the SCRN repeatedly tests the ability to recognize posterior danger signs independent of a low score.

Cerebellar danger signs and bedside action

Cerebellar strokes are not safe just because the patient can squeeze both hands. The posterior fossa has little room to swell, so a cerebellar infarct or hemorrhage can develop edema over hours to days, compress the fourth ventricle to cause obstructive hydrocephalus, and compress the brainstem. Severe occipital headache, repeated vomiting, inability to sit upright, new dysarthria, or decreasing arousal in a cerebellar patient are deterioration signs; routine antiemetics with delayed reassessment are unsafe when the neurologic trend is worsening, and these patients may need urgent neurosurgical decompression.

At the bedside: use BE-FAST fully, keep the patient safe from falls, hold oral intake until swallowing is screened, assess cough strength and voice quality (a wet, gurgly voice suggests an unsafe swallow), and report cranial nerve findings clearly. New dysphagia, drooling, weak cough, or decreasing arousal makes airway protection the priority. Separate benign dizziness from dangerous posterior patterns: isolated lightheadedness on standing differs from sudden continuous vertigo with diplopia, dysarthria, severe ataxia, or inability to walk unaided.

A focused posterior report includes eye movements, pupils, speech quality, voice wetness, cough strength, swallow status, limb coordination, truncal stability, gait if safely tested, headache, vomiting, and arousal, compared against the prior baseline because posterior deterioration can be abrupt.

The HINTS exam (Head-Impulse, Nystagmus, Test-of-Skew) is a clinician maneuver that, in acute continuous vertigo, can paradoxically be more sensitive than early imaging for a central (stroke) cause; central findings include a normal head-impulse test, direction-changing nystagmus, or skew deviation.

The nurse does not perform or interpret HINTS independently, but should know that an isolated normal CT does not exclude a posterior stroke, that continuous spontaneous vertigo with neurologic signs is high risk, and that escalation for specialist examination and MRI is appropriate rather than labeling the patient with benign peripheral vertigo and discharging.