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.
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.
Acute motor deficits occur in a wide range of disease states. 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.
There can be considerable overlap in presentations. For example, a sudden loss of motor function might often 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.
Motor deficits can be intermittent, relapsing, or acute and catastrophic, although these features do not always help define the pathophysiology.
- Transient ischaemic attack
- Ischaemic stroke
- Haemorrhagic stroke
- Traumatic brain injury
- Multiple sclerosis
- Focal nerve palsy
- Todd's paresis (postictal paralysis)
- Sleep disorders
- Subdural haematoma
- Subarachnoid haemorrhage (SAH)
- Thoracolumbar spine trauma
- Cervical spine trauma
- Brain abscess
- West Nile virus (WNV)
- Guillain-Barre syndrome (GBS)
- Myasthenia gravis (MG)
- 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
- Bell's palsy
Kenneth F. Casey, MD, FACS
Clinical Associate Professor PM&R
Wayne State University School of Medicine
KFC declares that he has no competing interests.
Cory Toth, BSc, MD, FRCP(C)
Assistant Professor of Neurosciences
Hotchkiss Brain Institute
University of Calgary
CT declares that he has no competing interests.
Sabrina Ravaglia, MD, PhD
Department of Neurological Sciences
Institute of Neurology C. Mondino
SR declares that she has no competing interests.
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