Aetiology

When trying to diagnose the cause of an acute motor deficit, the anatomical sites affected and the likely underlying pathophysiological cause should be considered. In general, the part of the neuromotor system involved should be identified first before attempting to identify the underlying pathology.

In broad terms, the site (or level) of dysfunction can be considered in the following terms:

  • Supraspinal lesions

  • Spinal cord lesions

  • Peripheral neuropathies

  • Disorders of neuromuscular transmission

  • Muscle disorders

Once the most likely site of the lesion is determined by the history and physical examination findings, it is necessary to consider the possible pathological processes. Each process will suggest specific diagnoses for the site/level concerned. By ordering the most appropriate tests and investigations, the search for a specific diagnosis can be narrowed. Broadly, the main categories to consider are:

  • Vascular causes

  • Trauma related

  • Infection

  • Autoimmune/inflammatory

  • Metabolic

  • Compression

  • Other

Vascular

Vascular causes of acute motor deficits frequently occur in the setting of known risk factors for atherosclerosis (e.g., hypercholesterolaemia, hypertension, diabetes mellitus, smoking), but may also occur spontaneously with embolic or occlusive events.

Stroke mimics have become increasingly recognised with the advent of intravenous tissue plasminogen activator (tPA) for stroke. The majority of stroke mimics are due to seizures, migraines, sepsis, conversion disorders, dementia and tumours.[1] Hypoglycaemia can also lead to focal motor deficits that mimic stroke.

Trauma

Traumatic processes (e.g., brain injury, spinal cord concussion, thoracolumbar or cervical spine injury) may cause acute motor deficit as a consequence of the primary injury (e.g., spinal cord transection) or as a late consequence of secondary injury (e.g., delayed intracranial haematoma or post-traumatic gliosis).[2] For example, a patient may present following a minor head injury with new hemiparesis or hemiplegia due to a subdural haematoma or obstructive hydrocephalus, consequent to the initial head injury.

Infection

Infectious causes are ubiquitous, but in some cases there are relevant seasonal and geographical considerations affecting organisms or vectors that increase or decrease the likelihood of particular types of infection. For example, infections with West Nile virus infection correlate with mosquito activity, peaking between July and October in temperate regions.[3]​

A helpful approach may be to categorise the process into 4 stages or causes: acute encephalopathy, chronic encephalopathy with exacerbation, toxin-mediated encephalopathy, and encephalopathy related to systemic illness. This process is predicated on the history supporting the possibility of an infectious agent, such as travel history or fever pattern.

Metabolic

Metabolic conditions that give rise to acute motor deficits can be difficult to identify in many cases. The brain, for example, is dependent on extracerebral systems for nutrients, waste clearance, and some protective functions, so disease states producing CNS dysfunction may originate in these extracerebral sites (e.g., liver, kidney, or heart). For instance, hypokalaemia may arise from renal, gastrointestinal, or endocrine dysfunction; absence of specific liver enzymes can give rise to glycogen storage diseases that may result in acute motor deficit; and defective or specifically absent glycoproteins in the membrane of the muscle wall can give rise to muscular dystrophies.

Autoimmune/inflammatory

There are several acute conditions in which rapid motor loss occurs due to an inflammatory reaction to central or peripheral nerves. Recognised syndromes of post-infectious or inflammatory reactions include acute disseminated encephalomyelitis, Guillain-Barre syndrome (GBS), and transverse myelitis.[4] 

Regarding GBS, the nomenclature has varied in the international literature.[4] Acute inflammatory demyelinating polyradiculoneuropathy (AIDP) is the most widely recognised form of GBS in western countries, but the variants known as acute motor axonal neuropathy (AMAN), acute motor-sensory axonal neuropathy (AMSAN), and Miller-Fisher syndrome also are well recognised. AIDP, AMAN, and AMSAN comprise the majority of cases in China, Japan, and Mexico.

In multiple sclerosis, the autoimmune phenomena produce demyelination and axonal disruption as a consequence of T-cell attack.

Compressive

Compression of nerves at any level of the nervous system can cause nerve dysfunction and give rise to motor deficit. Within the skull, this can be due to brain tumours (primary or metastatic), abscess formation, or hydrocephalus. The spinal cord can be compressed by disc prolapse, tumours, or an epidural abscess. Compartment syndrome of the limbs can cause both peripheral nerve dysfunction and muscle breakdown, giving rise to motor deficits.

Tumours that are intrinsic to the CNS account for 1.5% to 2.0% of all malignancies, but metastatic tumours affecting brain and spinal cord function occur in up to 17% of all people with cancer.[5] The most frequent tumours to metastasise to the CNS are lung, breast, melanoma, kidney, colon, and thyroid.

Other

There are many other processes that can produce acute motor deficit, whether due to ion abnormalities, seizures, or idiopathic cellular dysfunction. Fortunately, these are relatively rare situations, but they require additional thought to decipher the pattern of loss and determine the cause. For example, hypnagogical sleep paralysis (also known as isolated sleep paralysis) is diagnosed by the history of accompanying hallucinations.

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