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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.
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.
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.
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.
What are the vital signs?
Irregular heart rhythm may suggest cardioembolic stroke; fever may suggest an infectious process.
Maintain the patient at bed rest.
Use a chest restraint, if necessary, to prevent patients from injuring themselves.
If there has been trauma to the head or neck, stabilize the cervical spine with a cervical collar (see Chapter 7 , Spinal Cord Compression).
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.
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 |
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) |
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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