Gait Failure


The control of gait and posture involves numerous components of the nervous system. Gait ataxia implies decomposition in the coordinated control of posture and gait that are typically controlled by the cerebellum and other subcortical structures.

A call for a patient with gait failure requires consideration of a broad differential diagnosis. Successful evaluation begins with an assessment of the time course of the symptoms. Associated signs on examination will help with anatomic localization. Management may range from emergent neurosurgical decompression of a cerebellar hematoma to a thorough laboratory evaluation to seek a cause for a chronic degenerative disease.

Phone call

Questions

  • 1.

    When did the patient last walk normally?

    This is a key question from which your route of investigation and management begins.

    • Acute Onset: If the patient was known to have been walking normally within the past 24 hours, you must rule out stroke ( Chapter 6 ), spinal cord compression ( Chapter 7 ), traumatic brain injury ( Chapter 9 ), or a mass lesion in the posterior fossa ( Chapter 10 ). These are medical emergencies.

    • Subacute Onset: A subacute course (days to weeks) suggests an infectious, inflammatory, or neoplastic process.

    • Chronic Onset: If the gait deterioration has occurred over weeks to months, your differential diagnosis will be weighted toward degenerative processes, either inherited or acquired.

  • 2.

    Has there been any trauma to the head, neck, or back?

    A traumatic subdural hematoma or injury to the spinal cord or peripheral nerves may alter gait.

  • 3.

    What is the patient’s level of consciousness?

    Is the patient alert and awake, agitated, or confused? If a patient has an abnormal mental status in combination with ataxia or gait failure, acute intoxication or significant brain injury is likely.

  • 4.

    What are the vital signs?

    Irregular heart rhythm may suggest cardioembolic stroke; fever may suggest an infectious process.

Orders

  • 1.

    Maintain the patient at bed rest.

  • 2.

    Use a chest restraint, if necessary, to prevent patients from injuring themselves.

  • 3.

    If there has been trauma to the head or neck, stabilize the cervical spine with a cervical collar (see Chapter 7 , Spinal Cord Compression).

Elevator thoughts

What is the differential diagnosis of gait failure?

Gait failure may occur as a result of damage to almost any part of the neural axis. Your initial examination of the patient will help establish whether you are dealing with disturbance of motor, sensory, or cerebellar function. Table 11.1 is an outline of the categories of diseases that cause gait dysfunction and the characteristic features of the gait disturbance. Table 11.2 provides a more detailed differential diagnosis of ataxia.

Table 11.1
Clinical Features of Gait Disturbances
Disease Category Features of Gait Failure
Focal brain injury (hemiparesis) Spastically extended leg
Spastically flexed arm
Circumduction of paretic limb
Spinal cord injury (paraparesis) Stiff, effortful movements at knees and hips
Bilateral circumduction
Toe-walking or scissoring gait
Peripheral or central deafferentation (sensory ataxia) Wide-based stance and gait
High-stepping gait
Positive Romberg sign
Cerebellar disease Titubation (unsteady, oscillating posture) on sitting or standing
Wide-based stance and gait
Difficulty turning
Ataxia: staggering or lurching (unilateral or bilateral)
Normal-pressure hydrocephalus “Magnetic,” shuffling gait
Many steps taken to turn 180 degrees
Turning en bloc
Increased sway in stance
Start hesitation and freezing of gait
Slow gait speed with short steps
Lower motor neuron disease Distal weakness (e.g., foot drop)
High-stepping gait
Myopathy Proximal leg weakness
Difficulty arising from seated position
Difficulty climbing stairs
Parkinsonism Stooped posture
Shuffling gait
Retropulsion
Difficulty initiating and terminating
Freezing of gait “festinating gait”
Variable stepping
Slow, narrow base of support during gait
Reduced arm swing during gait
Congenital/perinatal (cerebral palsy) Hypertonic extended legs
Hypertonic flexed arms
Scissoring gait
Adventitial movements (abnormal posturing or movements of one or more limbs)
Multiple sclerosis Slow gait
Reduced endurance
Reduced stride length and joint motion
May see foot drop caused by weakness
Concussions Slow gait
Increased sway in frontal plane
Impairments worsen during divided attention (dual-task gait)
Dementia (vascular) Gait disorder occurs early in disease
Slow gait, short steps, and rigidity
Wide support base
Dementia (Alzheimer’s disease) Gait disorder occurs later in disease
Slow speed, short steps
Greater time on both feet
Variable stepping, especially when performing cognitive dual task
Cautious gait Slow speed, short steps
Extremely long time on both feet
“Walking on ice”: stiff lower limbs, outstretched arms
Linked with increased fear of falling

Table 11.2
Differential Diagnosis of Gait Failure by Mode of Onset
Modified from Harding AE. Ataxic disorders. In Bradley WG, Daroff RB, Fenichel GM, Marsden CD, eds. Neurology in Clinical Practice. Boston, MA: Butterworth-Heinemann; 1991.
Mode of Onset Disease Process
Acute (minutes to hours) Cerebellar hemorrhage
Cerebellar infarction
Acute intoxication
Head trauma
Basilar migraine
Dominant periodic ataxia (in children)
Benign paroxysmal positional vertigo
Subacute (hours to days) Posterior fossa tumor
Posterior fossa abscess
Multiple sclerosis
Toxins/intoxications
Hydrocephalus
Miller-Fisher variant of Guillain-Barré syndrome
Viral cerebellitis (mostly in children)
Chronic (days to weeks) Alcoholic cerebellar degeneration
Paraneoplastic cerebellar syndrome
Foramen magnum compression
Chronic infection (e.g., Jakob-Creutzfeldt disease, rubella, panencephalitis)
Hydrocephalus
Hypothyroidism
Vitamin E deficiency
Inherited ataxias (autosomal recessive or dominant)
Idiopathic degenerative ataxias
Episodic Recurrent intoxications
Multiple sclerosis
Transient ischemic attacks
Dominant periodic ataxia (children)

Major threat to life

  • Cerebellar hemorrhage or infarction

    Hematoma or infarction in the posterior fossa may progress to herniation and death if the lesion is large. It may require emergent neurosurgical evacuation.

  • Acute intoxication

    Intoxication with sedatives such as barbiturate or alcohol may present initially as ataxia and may lead to respiratory failure.

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