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Acute loss of strength, measured by the force of maximal contraction. Acute weakness can further be characterized by time course (fixed, fluctuating, or fatigable), pattern of muscle involvement, muscle bulk and tone, deep tendon reflexes (DTRs), sensory symptoms, muscle fasciculations, and bowel and bladder symptoms. Be sure to assess for common mimics, such as joint or bone pain causing refusal to walk or move, fatigue, and ataxia.

  • Muscle bulk: Assess symmetry of muscle bulk

  • Muscle tone: Assess by passive movement of limbs with patient relaxed; may be normal, increased (hypertonic: spastic or rigid), or decreased (hypotonic)

  • Strength and deep tendon reflexes: See Table 20-1.

Table 20-1Scales for Strength and DTRs

Etiology (By Localization)

  • Central nervous system (CNS), brain: Acute arterial ischemic stroke or transient ischemic attack, sinus venous thrombosis, inflammatory/demyelinating lesion (such as acute disseminated encephalomyelitis (ADEM) or multiple sclerosis), encephalitis, metabolic stroke, unilateral or bilateral

  • CNS, spinal cord (anterior horn-cell body): Cord infarction, cord compression (abscess, mass, venous malformation), trauma, contusion, infection (e.g., enterovirus), inflammatory/demyelinating lesions (transverse myelitis, ADEM, acute flaccid myelitis), spinal epidural abscess, syringomyelia

  • Spinal root of peripheral nerve: Acute inflammatory demyelinating polyneuropathy (Guillain–Barré syndrome [GBS])

  • Peripheral nerve (axon): Intensive care unit (ICU) neuropathy, human immunodeficiency virus (HIV) or zidovudine and certain antiretroviral therapies (zalcitabine, didanosine, lamivudine, stavudine), hereditary tyrosinemia, acute intermittent porphyria, medication-related (e.g., phenytoin, vincristine, nitrofurantoin, isoniazid), toxins (heavy metals, glue), metabolic (uremia-mixed sensory and motor, or pure motor after dialysis), autoimmune (lupus), other vasculitis, chronic juvenile rheumatoid arthritis

  • Neuromuscular junction: Myasthenia gravis, botulism, tic paralysis, pharmacologic blockade, aminoglycoside toxicity

  • Muscle: Myositis (infectious, dermatomyositis, polymyositis), metabolic (hypocalcemia, hypokalemia, hypothyroid state), medication-related (especially steroids), ICU myopathy, familial periodic paralysis (primary or secondary hypo/hyperkalemic)

Clinical Manifestations

  • See Table 20-2 for expected examination findings by location.

  • CNS, brain: Unilateral or bilateral (depending on etiology and distribution) weakness, sometimes in a cerebrovascular distribution (e.g., arterial ischemic stroke), but not always. May have concomitant encephalopathy, language, cranial nerve, or sensory changes; initial low tone then spastic; extensor plantar response (“upgoing toe”) on affected side (Table 20-2).

  • CNS, spinal cord: Acute flaccid paralysis (“spinal shock”; spasticity develops over time), bowel or bladder symptoms, incontinence, evolving spasticity, sensory level, back pain or trauma, with or without fasciculations, fever (epidural abscess), hypotension (infarction), decreased rectal tone, extensor plantar response (“upgoing toe”)

  • Spinal root of peripheral nerve: Symmetric length-dependent weakness, often ...

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