Q4 LONG ANSWER 10M ★ High-yield

Discuss the clinical approach to a patient presenting with acute flaccid paralysis or quadriparesis.

General Medicine · Final Professional

Definition

Acute flaccid paralysis (AFP) is the rapid onset (over hours to days) of weakness with hypotonia and reduced or absent reflexes, in the absence of upper motor neurone signs. Quadriparesis is weakness of all four limbs, which may be flaccid (acute) or spastic (chronic or after the phase of spinal shock).

The first task is to localise the lesion, since this determines the entire differential and the investigations.

Localisation — the Key Step

Site	Weakness Pattern	Reflexes	Sensation	Additional Clues
Anterior horn cell (poliomyelitis, West Nile, enterovirus)	Asymmetrical, patchy, proximal	Absent	Normal	Fever at onset, fasciculations, no sensory loss
Peripheral nerve (GBS, diphtheria, porphyria, toxins)	Symmetrical, ascending, distal to proximal	Absent early	Glove-and-stocking, or minimal	Cranial nerve and autonomic involvement in GBS
Neuromuscular junction (myasthenia, botulism, organophosphate)	Fatigable; bulbar and ocular prominent	Normal	Normal	Ptosis, diplopia; descending in botulism; pupils spared in MG, dilated in botulism
Muscle (periodic paralysis, myositis, rhabdomyolysis)	Proximal, symmetrical	Normal or reduced	Normal	Raised CK; potassium abnormality
Spinal cord (compression, transverse myelitis, trauma, infarct)	Para- or quadriparesis with a sensory LEVEL	Absent in spinal shock, later brisk with extensor plantars	Sensory level — the critical sign	Bladder and bowel involvement, back pain

CLINICAL PEARL

Three questions localise almost every case at the bedside. (1) Is there a sensory level? — if yes, the cord is the site until proved otherwise, and imaging is urgent. (2) Is the bladder involved? — early sphincter disturbance points to the cord, not to nerve or muscle. (3) Is the weakness ascending or descending? — ascending suggests GBS, descending suggests botulism or brainstem disease.

The Major Causes

1. Guillain–Barré syndrome — the commonest cause of AFP in adults worldwide; ascending symmetrical weakness with areflexia, preceded by infection.

2. Hypokalaemic periodic paralysis — very common in India and frequently the answer in an examination case. Sudden proximal weakness on waking or after a heavy carbohydrate meal or exertion, with preserved sensation, normal bulbar and respiratory function early, and profound hypokalaemia. Causes include thyrotoxic periodic paralysis (notably in Asian men), renal tubular acidosis (distal RTA), Gitelman and Bartter syndromes, diuretic and steroid use, and familial channelopathy. It reverses dramatically with cautious potassium replacement.

3. Transverse myelitis and cord compression — sensory level, sphincter involvement, back pain. Compression is a neurosurgical emergency.

4. Poliomyelitis and other enteroviruses — asymmetrical, pure motor, febrile at onset. All AFP under 15 years must be reported and investigated under the national AFP surveillance programme, with two stool samples for poliovirus — a public health obligation and an examination point.

5. Traumatic and vascular cord lesions; anterior spinal artery syndrome (loss of power and spinothalamic sensation with preserved dorsal columns).

6. Others: diphtheritic neuropathy (palatal palsy with accommodation paresis after a membranous pharyngitis), acute intermittent porphyria (abdominal pain, psychiatric features, motor neuropathy), toxic — organophosphate intermediate syndrome, snake envenoming (krait, cobra), heavy metals; tick paralysis; critical illness polyneuropathy and myopathy in ICU patients; and rhabdomyolysis.

Clinical Evaluation

History:

speed of onset and progression
ascending or descending
preceding fever, diarrhoea or respiratory infection
vaccination and travel history
back pain
bladder and bowel function
diurnal fluctuation and fatigability
dietary or exertional trigger
drug, toxin and alcohol exposure
snake bite
family history.

Examination:

tone, power (graded), reflexes and plantars
search deliberately for a sensory level, and record it
cranial nerves including pupils and bulbar function
respiratory assessment with single-breath count and forced vital capacity
autonomic signs (blood pressure lability, arrhythmia)
palpate the bladder.

Investigations

Immediate: serum potassium (hypokalaemic paralysis is instantly treatable), sodium, calcium, magnesium, creatine kinase, renal function, glucose, arterial blood gas, and ECG (U waves in hypokalaemia).
Spinal MRI urgently if there is any sensory level, bladder involvement or back pain — cord compression must be excluded within hours.
CSF examination: albuminocytological dissociation (high protein, normal cells) supports GBS; pleocytosis suggests infection, poliomyelitis or transverse myelitis.
Nerve conduction studies and EMG — distinguish demyelinating from axonal neuropathy, and neuropathy from myopathy and NMJ disease; repetitive nerve stimulation for myasthenia and botulism.
Thyroid function (thyrotoxic periodic paralysis); urine porphobilinogen; stool for poliovirus in children; antiganglioside antibodies; toxicology.

Management Principles

1. Protect the airway and breathing first. Monitor FVC and single-breath count serially; intubate on trend of deterioration, not on blood gases.

2. Correct reversible metabolic causes immediately — potassium, calcium, magnesium.

3. Exclude and treat cord compression as a surgical emergency.

4. Disease-specific therapy — IVIG or plasma exchange for GBS, immunotherapy for myasthenia and transverse myelitis, antivenom for envenoming, atropine and oximes for organophosphate poisoning.

5. Supportive care: DVT prophylaxis, pressure area care, bladder and bowel management, nutrition, physiotherapy to prevent contractures, pain management, and psychological support.

DANGER / REMEMBER

Respiratory failure is the killer in every cause of acute flaccid paralysis, and it develops silently. Oxygen saturation and arterial blood gases stay normal until the patient is close to arrest — because ventilatory failure from muscle weakness produces hypercapnia late. Monitor the forced vital capacity (or, at the bedside, ask the patient to count aloud in one breath) every few hours, and intubate on a falling trend.

All questions in Neurology / CNS

Every General Medicine chapter →