Your next patient is a 36-year-old man with weakness and numbness spreading over 3 days. Here's how the Guillain-Barre syndrome case unfolds and what to pick up on the way.

This guillain-barre syndrome case is easy to get wrong in the history because early sensory symptoms can distract from the pattern of symmetrical weakness. The timeline, a few days of tingling in a glove and stocking pattern followed by weakness climbing from the legs, often comes after a recent diarrhoeal illness, yet breathlessness that's worse lying flat and a nasal, slurred voice can shift focus away from the limbs. This page walks through how the 36-year-old man presents, what to pick up in the history and on examination, and the tests that support the diagnosis: CSF analysis, nerve conduction studies and MRI spine. Teaching points include the evolving flaccid weakness with absent knee reflexes, the albuminocytological dissociation caveat, and the risk of autonomic instability with labile blood pressure and arrhythmias.

How the case presents

Your next patient is a 36-year-old man with weakness and numbness spreading over 3 days. In their own words: "Weakness and numbness that's been spreading over the last few days."

Observations on arrival:

Observation	On arrival
Heart rate	108 beats per minute
Blood pressure	158/96 mmHg
Respiratory rate	22 breaths per minute
Oxygen saturation	96%
Temperature	37 °C

What to pick up in the history

These are the findings the case is built around. Each one moves you towards or away from Guillain-Barre syndrome, and the scorecard checks whether you found it.

Tingling and numbness in a glove-and-stocking pattern: distal symmetrical sensory symptoms point to a peripheral polyneuropathy rather than a cord or brain lesion.
Symmetrical weakness ascending from the legs upward: ascending symmetrical flaccid weakness is the defining pattern of Guillain-Barre syndrome.
Diarrhoeal illness about two weeks ago: an antecedent Campylobacter-type gut infection is the classic trigger and strongly supports the diagnosis.
Breathless, worse lying flat, cannot take a deep breath: diaphragmatic weakness threatens respiratory failure, the main killer, and mandates serial forced vital capacity.
Difficulty swallowing with slurred, nasal speech.
Knee reflexes absent when tapped: areflexia with weakness confirms a lower motor neurone process and excludes cord compression.
No bladder or bowel disturbance, normal saddle sensation: intact sphincters and saddle sensation argue strongly against cauda equina syndrome or cord compression.
Weakness worsening steadily over about five days.

Red flags you must not miss

The case marks these as must-elicit. They only come out if you ask.

Breathless, worse lying flat, cannot take a deep breath.
Difficulty swallowing with slurred, nasal speech.
He has had palpitations, sweating and light-headedness, with his heart racing at times.
Weakness worsening steadily over about five days.

Investigations and what they showed

CSF analysis: Raised protein with a normal white-cell count, albuminocytological dissociation (may be normal in the first few days). Why it helps: the classic CSF finding of GBS, high protein with few/no cells; a raised cell count would instead suggest infection or an alternative diagnosis. It can be normal very early, so a normal result does not exclude GBS.
Spirometry: Reduced and falling forced vital capacity (FVC) on serial measurement.
Nerve conduction studies: Features of a demyelinating polyradiculoneuropathy, slowed conduction velocities, prolonged distal latencies, conduction block and prolonged/absent F-waves. Why it helps: confirms the peripheral, demyelinating nature of the weakness and supports GBS (though changes can lag early on).
MRI whole spine: Smooth enhancement (± thickening) of the cauda equina / anterior spinal nerve roots after contrast. Why it helps: supports the diagnosis of an inflammatory polyradiculoneuropathy and excludes the key structural mimics, spinal cord compression and cauda equina syndrome, in a patient with rapidly progressive weakness.
Inspect the work of breathing: Breathing rapidly and shallowly at 22/min, speaking in short phrases, and when he lies flat the abdomen sucks in as the chest rises, paradoxical abdominal breathing. Why it helps: paradoxical abdominal movement means the diaphragm is failing, and this is the most important observation in the case.
Inspect the face: Both sides of the face are weak, the smile is flat on both sides, the eyes close only weakly, and the face looks expressionless rather than droopy on one side. Why it helps: bilateral facial weakness is a well-recognised feature of GBS. Because it is symmetrical it is easy to miss, nothing looks 'crooked', the face just looks blank, yet it flags bulbar involvement and airway risk.
Inspect the patient's gait: He walks unsteadily with a wide base, has to be helped to stand from the chair, and lifts his knees high because the feet slap the floor. Why it helps: the high-stepping slapping gait of bilateral foot drop with proximal weakness on standing is the visible expression of ascending symmetrical weakness, and the fact it has climbed from feet to thighs to trunk over days is the diagnosis.
Inspect the feet: Both feet hang down and cannot be pulled up against gravity, symmetrical bilateral foot drop. Why it helps: symmetrical, bilateral involvement distinguishes GBS from a common peroneal nerve palsy or a radiculopathy, which would be one-sided.
Inspect the patient's posture and position: He is sitting bolt upright, propped forward on pillows, and becomes distressed when asked to lie flat. Why it helps: orthopnoea in a neuromuscular patient is diaphragm weakness, not heart failure, a patient who will not lie flat is telling you his vital capacity is falling.
Inspect the mouth and oral cavity: Saliva pools in the mouth, he swallows with visible effort and his voice sounds nasal. Why it helps: pooling secretions and a nasal voice are bulbar weakness, an unprotected airway and a high aspiration risk. Together with a falling FVC this is the trigger to move to intensive care.

Imaging findings

ECG (bedside 12-lead): May show sinus tachycardia or arrhythmia; part of monitoring for autonomic instability.
CT head: No haemorrhage, infarct or mass. Normal.

Why the diagnosis is Guillain-Barre syndrome

The decisive diagnosis is guillain-barrÉ syndrome (GBS), an acute, post-infectious, immune-mediated demyelinating polyradiculoneuropathy: an ascending, symmetrical, flaccid weakness with areflexia and sensory symptoms, developing over days to a few weeks (usually 1 to 3 weeks after a Campylobacter or respiratory infection), often with pain, autonomic instability and, dangerously, bulbar and respiratory muscle involvement. Confirm with CSF (albuminocytological dissociation) and nerve conduction studies, and, most importantly, monitor the forced vital capacity, because respiratory failure is the main killer and SpO2 drops late. Distinguish it from myasthenia gravis (fatigable, ocular/bulbar, reflexes preserved), spinal cord compression / cauda equina (a sensory level, sphincter involvement, UMN signs), hypokalaemia, and CIDP (the chronic form, >8 weeks).

Guillain-Barre syndrome at a glance

What it is

Guillain-Barre syndrome (GBS) is an acute, immune-mediated polyradiculoneuropathy that usually follows an infection by one to three weeks. It causes ascending, symmetrical, flaccid weakness with loss of reflexes and sensory symptoms, evolving over days to a few weeks.

Pathogenesis

An antecedent infection, classically Campylobacter jejuni, triggers an immune response whose antibodies cross-react with components of peripheral nerve myelin (molecular mimicry). This immune attack strips the myelin sheath from peripheral nerves, slowing or blocking nerve conduction and producing progressive, ascending weakness, sensory symptoms and loss of reflexes. Because the nerves supplying respiratory and bulbar muscles can be affected, the diaphragm and swallowing can fail well before oxygen levels drop, which is why monitoring breathing directly, rather than waiting for hypoxia, is essential.

Who it affects

GBS can affect any age but is more common in adults, and slightly more common in men. It typically follows a Campylobacter jejuni gastrointestinal infection or a respiratory infection by one to three weeks.

How serious it is

GBS is potentially life-threatening: respiratory failure from diaphragm weakness is the main cause of death, alongside autonomic instability that can cause dangerous arrhythmias or blood pressure swings.

Causes and risk factors

Campylobacter jejuni gastroenteritis is the classic antecedent infection, though respiratory infections and other triggers are also recognised.

Investigations and lab tests

Nerve conduction studies confirm a demyelinating polyneuropathy. CSF analysis classically shows albuminocytological dissociation (raised protein with a normal cell count), but can be normal in the first few days. An MRI spine can support the diagnosis (enhancing nerve roots) and helps exclude cord compression or cauda equina syndrome. Above all, serial forced vital capacity must be measured regularly, since it is the best predictor of impending respiratory failure.

At a glance: Confirms diagnosis: nerve conduction studies. Supports it: CSF (albuminocytological dissociation, may be normal early). Most important ongoing test: serial forced vital capacity.

Teaching points

Guillain, Barré syndrome is an acute, post-infectious immune polyradiculoneuropathy, ascending symmetrical flaccid weakness with areflexia and sensory symptoms, evolving over days to weeks (usually 1 to 3 weeks after Campylobacter or a respiratory infection).
CSF shows albuminocytological dissociation (raised protein, normal cells), but it can be normal in the first few days, so a normal CSF does not exclude GBS.
Nerve conduction studies confirm a demyelinating polyneuropathy; an MRI spine (enhancing cauda equina/nerve roots) supports GBS and excludes cord compression/cauda equina.
Autonomic instability (labile BP, arrhythmias) is common and can be fatal, keep the patient on continuous cardiac monitoring.
Distinguish GBS from myasthenia gravis (fatigable, ocular/bulbar, reflexes preserved), spinal cord compression/cauda equina (sensory level, sphincter signs, UMN signs), hypokalaemia, and CIDP (chronic, >8 weeks).

Practise a similar case

Reading a tidy case is not the same as finding the thread yourself under a bit of pressure. It feels different when you are the one who has to ask and then notice that the knee reflexes are absent when tapped. Try the next neurology history.

Here's one from the same specialty, with the diagnosis left for you to find. Your next patient is 64 and had another fit last night after a similar episode 2 weeks ago. Take this patient's history in Diagnosica. It's free to start, no card needed.

Guillain-Barre syndrome case presentation: history, findings and tests