Assessment of acute motor deficit

Last reviewed: December 2018

Last updated: June 2018

Summary

Acute motor deficits occur when there is either a sudden loss of connectivity between the central nervous system (CNS) and the muscles or there is dysfunction of the muscles themselves. Loss of connection can occur anywhere from the CNS to the motor-end plate. Acute motor deficits occur in a wide range of disease states. Careful questioning of a patient who reports sudden motor loss can help determine the exact anatomy of the motor deficit, any accompanying features, and the likely pathophysiology. The anatomical description of the deficit helps localise the site of dysfunction. This may include the brain, spinal cord, peripheral nerves, and muscles. Motor deficits can be intermittent, relapsing, or acute and catastrophic, although these features do not always help define the pathophysiology.

Once the probable site of dysfunction has been identified, consideration can be given to the likely type of process involved (vascular, trauma, infection, autoimmune/inflammatory, metabolic, compression, or other). Although a general knowledge of the different systemic pathologies is helpful, there can be considerable overlap in presentations. For example, a sudden loss of motor function might often appear to have a vascular cause, but other conditions, such as oedema related to a tumour in the white matter or chronic subdural haematoma, can present with a similar history, albeit less frequently.

Differentials

Common

Transient ischaemic attack
Ischaemic stroke
Haemorrhagic stroke
Traumatic brain injury
Multiple sclerosis
Hypoglycaemia
Focal nerve palsy
Todd's paresis (postictal paralysis)
Sleep disorders

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Uncommon

Subdural haematoma
Subarachnoid haemorrhage (SAH)
Haematomyelia
Thoracolumbar spine trauma
Cervical spine trauma
Encephalitis
Brain abscess
Coxsackievirus
West Nile virus (WNV)
Diphtheria
Poliovirus
Guillain-Barre syndrome (GBS)
Myasthenia gravis (MG)
Vasculitis
Transverse myelitis (TM)
Idiopathic inflammatory myopathy
Acute hypokalaemia
Acute intermittent porphyria (AIP)
Periodic paralysis
Amyotrophic lateral syndrome
Muscular dystrophies
Common hereditary lysosomal storage diseases
Type 1 glycogen storage disease (GSD I)
Drug-induced myopathies
Drug-induced neuropathy
Toxin-induced dysfunction
Compartment syndrome
Brain tumour
Spinal cord compression
Hydrocephalus
Bell's palsy

Full details

Contributors

Authors VIEW ALL 

Kenneth F. Casey, MD, FACS

Clinical Associate Professor PM&R

Wayne State University School of Medicine

Detroit

Disclosures

KFC declares that he has no competing interests.

Peer reviewers VIEW ALL 

Cory Toth, BSc, MD, FRCP(C)

Assistant Professor of Neurosciences

Hotchkiss Brain Institute

University of Calgary

Alberta

Canada

Disclosures

CT declares that he has no competing interests.

Sabrina Ravaglia, MD, PhD

Staff Physician

Department of Neurological Sciences

Institute of Neurology C. Mondino

Pavia

Italy

Disclosures

SR declares that she has no competing interests.

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Assessment of acute motor deficit

Summary

Differentials

Common

Uncommon

Contributors

Authors VIEW ALL 

Kenneth F. Casey, MD, FACS

Disclosures

Peer reviewers VIEW ALL 

Cory Toth, BSc, MD, FRCP(C)

Disclosures

Sabrina Ravaglia, MD, PhD

Disclosures

Patient leaflets

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