Acute Non-Traumatic Weakness

Reviewed and revised 13 April 2016


Acute non-traumatic weakness may occur as a result of a wide variety of underlying etiologies, many of which are life-threatening

  • Key considerations include:
    • assessment of the need for intubation and respiratory support
    • identification of time-critical emergencies
    • determination of the underlying cause, based on clinical assessment and investigations, including a careful physical examination to facilitate neurological localisation and diagnosis



  • Increasing generalized muscle weakness
  • Dysphagia
  • Dysphonia
  • Dyspnea on exertion and at rest


  • Rapid shallow breathing
  • Tachycardia
  • Weak cough
  • Interrupted speech (gasping for air)
  • Use of accessory muscles
  • Abdominal paradoxical breathing
  • Orthopnea
  • Weakness of trapezius and neck muscles: inability to lift head from bed
  • Inability to perform single-breath count: count from 1 to 10 in single exhalation (roughly equal to FVC <1.0 L)
  • Cough after swallowing


  • Decreased level of consciousness (have a lower threshold to control the airway if patient requires transfer or movement to unmonitored areas)
  • Hypoxemia
  • Vital capacity <1 L or 20 mL/kg, or 50 % decrease in VC in a day
  • Maximum inspiratory pressure >-30 cm H2O
  • Maximum expiratory pressure <40 cm H2O
  • Hypercapnia (occurs late)

Base the decision to intubate on a global overview of the above factors – not any single parameter – and take into account the time course and anticipated trajectory of illness

  • reassess the patient frequently
  • intervene before the onset of hypercapnia if possible


These include:

  • stroke syndromes
  • aortic dissection
  • CNS infections
  • spinal cord syndromes
  • seizure disorders
  • envenoming (e.g. snake)
  • acute toxicity e.g. organophosphates, heavy metals
  • electrolyte/ metabolic disorders



  • Myopathic – rhabdomyolysis, ischaemic, congenital, CIW
  • NMJ – myasthenia gravis, botulism
  • Neuropathic – GBS, CIW, polio
  • Spinal Cord – infarct, infection, tumour
  • Brain stem – haemorrhage, infarct, infection, mass lesion
  • Brain – haemorrhage, infarct, infection, tumour
  • Systemic – organ failures, electrolytes, sepsis, toxins


  • Acute stroke: ischemic, hemorrhagic, or subarachnoid hemorrhage
  • Intracranial mass
  • Meningitis/encephalitis
  • Hypoglycemia/hyperglycemia
  • Postictal Todd’s paresis
  • Hemiplegic migraine
  • Brown-Sequard syndrome

Quadriparesis/Paraparesis ± Sensory Level

  • Spinal cord compression
  • Spinal cord infarction
  • Transverse myelitis

Proximal Weakness

  • Acute myopathy
  • Guillain–Barré syndrome (GBS)
  • Diabetic lumbosacral radiculoplexus neuropathy (DLRN)
  • Myasthenia gravis
  • Lambert-Eaton myasthenic syndrome (LEMS)

Distal Weakness

  • Vasculitic neuropathy
  • Toxin induced peripheral neuropathy
  • Nerve compression syndromes

Any severe medical illness may have weakness as a presenting symptom, and psychiatric diagnoses may also mimic neuromuscular disorders


Clinical assessment

  • Relevant history
  • Examination
    • systemic features
    • neurological examination (see neurological localisation, below)


  • Laboratory
    • glucose, electrolytes, Ca, Mg, PO4, UEC, LFTs, and coags
    • TFTs, CK, ESR
    • others according to suspected etiology: e.g. CSF, vasculitis screen
  • Imaging (according to suspected etiology)
    • CTB, CTB +/- contrast +/- angiogram +/- venogram
    • MRI brain +/- angiography
    • CT or MRI spine


LocalisationPattern of weaknessSensory lossReflexesAcute causes
Cerebral cortex, brainstem, or spinal cordDistal > proximal, extensors > flexors, hemiparesis or single limbMay be present depending on whether sensory tracts or cortex are involvedIncreased (may be decreased initially)Acute stroke, SAH, seizure, hypertensive encephalopathy
Spinal cordDistal > proximal, extensors > flexors, paraparesis, quadriparesis, rarely hemiparesisIncreased (may be decreased initially)Epidural abscess, tumor, spinal cord infarct
Anterior horn cellProximal and distal, fasciculations are prominentabsentDecreased if muscle bulk is severely decreased; increased in ALSALS, polio
Peripheral nerveIn the distribution of the nerve, or diffusely present as stocking/glove weaknessPresentDecreasedGuillain-Barre Syndrome
Neuromuscular junctionFirst in eye muscles, neck extensors, pharynx, diaphragm, followed by more generalized weaknessAbsentNormal, decreased if muscle is paralyzedBotulism, tick bite, organophosphates
MuscleProximalAbsentNormal unless muscle severely weakRhabdomyolysis
  • However, in the acute phase, UMN lesions may be difficult to differentiate from a LMN lesion
    • acute UMN lesions may result in flaccid paralysis, normal or reduced tone, and unreliable reflexes
    • in acute LMN lesions there may be insufficient time for atrophy to be evident and fasciculations are rarely seen


Airway and respiratory management

  • Assess for intubation (see factors to consider, above)
    • key life threats are:
      • airway obstruction due to oropharyngeal collapse
      • respiratory failure due to diaphragmatic weakness
      • respiratory failure due to aspiration from inadequate airway protection
  • Non-invasive ventilation
    • Consider as a temporizing measure in a neurologically stable patient with a neuromuscular condition expected to have rapid resolution (e.g., myasthenia gravis exacerbation)
    • Consider use for pre-oxygenation prior to intubation
  • Avoid suxamethonium if there is evidence of underlying progressive neuromuscular disease (e.g., Guillain-Barre Syndrome, chronic muscular weakness, or prolonged immobility) — use rocuronium (1.2 mg/kg IV IBW) for rapid sequence intubation
  • Myasthenia gravis
    • Succinylcholine is relatively ineffective, double the standard dose if used (e.g. 3 mg/kg IV)
    • Alternatively, use  half-dose of non-depolarizing agents (e.g. rocuronium 0.6 mg/kg IV IBW)
  • If autonomic instability is present or anticipated
    • Prepare atropine/glycopyrrolate, fluids, and vasopressors prior to intubation
    • anticipate swings and avoid overshoot (i.e. don’t chase hypotension too aggressively with vasopressors, as there may be a dramatic swing to severe hypertension as a result of autonomic instability)

Specific therapy

  • according to underlying cause

Supportive care and monitoring

References and Links


Journal articles

  • Flower O, Bowles C, Wijdicks E, Weingart SD, Smith WS. Emergency neurological life support: acute non-traumatic weakness. Neurocrit Care. 2012 Sep;17 Suppl 1:S79-95. PMID: 22972018.

CCC 700 6

Critical Care


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