Gait Disorders, Imbalance, and Falls¶
Chapter 28 | Part 2: Cardinal Manifestations and Presentation of Diseases
KEY CLINICAL POINTS¶
- Gait disorders affect 15% of individuals aged >65 and up to 40% of those aged ≥ 85, representing a major risk factor for falls and injury
- Balance depends on integration of visual, vestibular, and proprioceptive sensory systems—loss of two of three pathways compromises standing balance
- Neurologic gait disorders can be classified by etiology: sensory ataxic (most common single disorder at 18%), parkinsonian (16%), higher-level/frontal (8%), cerebellar ataxic (6%), and others
- Falls affect over one-third of community-dwelling adults aged >65 annually, with hip fractures associated with substantially increased mortality risk in the subsequent year
- Multifactorial assessment and intervention targeting modifiable risk factors (medications, vision, strength, environment) reduces fall risk in older adults
1. DEFINITION & OVERVIEW¶
Upright bipedal gait depends on successful integration of postural control and locomotion, functions that are widely distributed in the central nervous system. The biomechanics of bipedal walking are complex and easily compromised by neurologic deficit at any level. Command and control centers in the brainstem, cerebellum, and forebrain modify the action of spinal pattern generators to promote stepping. Step generation in primates is dependent on locomotor centers in the pontine tegmentum, midbrain, and subthalamic region. Locomotor synergies are executed through the reticular formation and descending pathways in the ventromedial spinal cord. Cerebral control provides goal and purpose for walking and is involved in obstacle avoidance and adaptation of locomotor programs to context and terrain.
1.1 Postural Control Mechanisms¶
Postural control requires maintenance of the center of mass over the base of support through the gait cycle. Unconscious postural adjustments maintain standing balance with long latency responses measurable in leg muscles beginning 110 milliseconds after perturbation. Forward motion of the center of mass provides propulsive force for stepping, but failure to maintain the center of mass within stability limits results in falls. The vestibular nucleus and midline cerebellum contribute to balance control; damage to these structures impairs balance while standing and walking.
1.2 Sensory Requirements for Balance¶
Standing balance depends on good-quality sensory information about the position of the body center with respect to the environment, support surface, and gravitational forces. Sensory information for postural control is primarily generated by: (1) the visual system, (2) the vestibular system, and (3) proprioceptive receptors in muscle spindles and joints. A healthy redundancy of sensory afferent information is generally available, but loss of two of three pathways is sufficient to compromise standing balance.
1.3 Cognitive Contributions to Gait¶
Walking is generally considered unconscious and automatic, but the ability to walk while attending to a cognitive task (dual-task walking) may be compromised in the elderly. Older patients with deficits in executive function may have particular difficulty managing attentional resources needed for dynamic balance when distracted. Decline in gait speed and memory are increasingly associated with risk for dementia in older adults. Patients with cognitive impairment appear particularly prone to falls and injury.
2. EPIDEMIOLOGY¶
Gait and balance problems are common in the elderly and contribute significantly to the risk of falls and injury. The prevalence of gait disorders increases dramatically with advancing age.
2.1 Prevalence by Age¶
Gait disorders have been described in 15% of individuals aged >65. By age 80, one person in four (25%) will use a mechanical aid to assist with ambulation. Among those aged ≥ 85, the prevalence of gait abnormality approaches 40%.
2.2 Falls Epidemiology¶
Over one-third of people aged >65 living in the community fall each year; this number is even higher in nursing homes and hospitals. Elderly people are not only at higher risk for falls but also more likely to suffer serious complications due to medical comorbidities such as osteoporosis. The proportion of spinal cord injuries due to falls in individuals aged >65 has doubled in the past decade, perhaps due to increasing activity in this age group.
2.3 Impact on Quality of Life¶
Nearly one in five elderly individuals voluntarily restricts their activity because of fear of falling. With loss of ambulation, quality of life diminishes and rates of morbidity and mortality increase. Hip fractures result in hospitalization, can lead to nursing home admission, and are associated with substantially increased mortality risk in the subsequent year.
3. ETIOLOGY & PATHOPHYSIOLOGY¶
Disorders of gait may be attributed to neurologic and nonneurologic causes, with significant overlap often existing. The heterogeneity of gait disorders observed in clinical practice reflects the large network of neural systems involved in the task. Walking is vulnerable to neurologic disease at every level.
Prevalence of Neurologic Gait Disorders¶
| Neurologic Gait Disorder | No. (%) | Total Number | Causes (No.) |
|---|---|---|---|
| Single neurologic gait disorder | 81 (69%) | ||
| Sensory ataxic | 22 (18%) | 46 | Peripheral sensory neuropathy (46) |
| Parkinsonian | 19 (16%) | 34 | Parkinson's disease (18), drug-induced parkinsonism (8), dementia with parkinsonism (4), parkinsonism (4) |
| Neurologic Gait Disorder | No. (%) | Total Number | Causes (No.) |
|---|---|---|---|
| Higher level | 9 (8%) | 31 | Vascular encephalopathy (20), normal pressure hydrocephalus (1), severe dementia (7), hypoxic ischemic encephalopathy (1), unknown (1) |
| Cerebellar ataxic | 7 (6%) | 10 | Cerebellar stroke (3), cerebellar lesion due to MS (1), severe essential tremor (3), postvaccinal cerebellitis (1), chronic alcohol abuse (1), MSA (1) |
| Cautious | 7 (6%) | 7 | Idiopathic, associated fear of falling (7) |
| Paretic/hypotonic | 6 (5%) | 14 | Neurogenic claudication (7), diabetic neuropathy (1), nerve lesion due to trauma/surgery (4), distal paraparesis after GBS (1), unknown (2) |
| Spastic | 6 (5%) | 7 | Ischemic stroke (3), intracerebral hemorrhage (3), congenital (1) |
| Vestibular ataxic | 4 (3%) | 6 | Bilateral vestibulopathy (3), recent vestibular neuronitis (1), recent Ménière's attack (1), acoustic neuroma with surgery (1) |
| Dyskinetic | 1 (1%) | 4 | Levodopa-induced dyskinesia (3), chorea (1) |
| Multiple neurologic gait disorders | 36 (30%) | ||
| Total | 117 |
3.1 Nonneurologic Causes¶
The antalgic gait results from avoidance of pain associated with weight bearing and is commonly seen in osteoarthritis. Asymmetry is a common feature of gait disorders due to contractures and other orthopedic deformities. Impaired vision rounds out the list of common nonneurologic causes of gait disorders.
3.2 Neurologic Classification¶
Gait disorders have been classified descriptively based on abnormal physiology and biomechanics. One problem with this approach is that many failing gaits look fundamentally similar. This overlap reflects common patterns of adaptation to threatened balance stability and declining performance. The gait disorder observed clinically must be viewed as the product of a neurologic deficit and a functional adaptation; unique features are often overwhelmed by the adaptive response.
3.3 Age-Related Multiple Insults¶
Balance disorders in older individuals sometimes result from multiple insults in peripheral sensory systems (visual loss, vestibular deficit, peripheral neuropathy) that critically degrade the quality of afferent information needed for balance stability.
4. CLINICAL FEATURES¶
Multiple distinct patterns of gait abnormality can be recognized clinically, each with characteristic features that may suggest underlying etiology. Understanding these patterns is essential for diagnosis and management.
Features of Cerebellar Ataxia, Sensory Ataxia, and Frontal Gait Disorders¶
| Feature | Cerebellar Ataxia | Sensory Ataxia | Frontal Gait |
|---|---|---|---|
| Base of support | Wide-based | Wide-based, looks down | Wide-based |
| Velocity | Variable | Slow | Very slow |
| Stride | Irregular, lurching | Regular with path deviation | Short, shuffling |
| Romberg test | +/- | Unsteady, falls | +/- |
| Heel fi shin | Abnormal | +/- | Normal |
| Initiation | Normal | Normal | Hesitant |
| Turns | Unsteady | +/- | Hesitant, multistep |
| Postural instability | + | +++ | ++++ Poor postural synergies rising from chair |
| Falls | Late event | Frequent | Frequent |
4.1 Cautious Gait¶
Characterized by abbreviated stride, widened base, and lowered center of mass, as if walking on a slippery surface. Arms are often held abducted. This disorder is both common and nonspecific—essentially an adaptation to perceived postural threat. There may be an associated fear of falling. Can be observed in more than one-third of older patients with gait impairment. Physical therapy often improves walking; follow-up observation may reveal a more specific underlying disorder.
4.2 Stiff-Legged (Spastic) Gait¶
Characterized by stiffness in legs, imbalanced muscle tone, and tendency to circumduct and scuff feet. Reflects compromise of corticospinal command and overactivity of spinal reflexes. Patient may walk on toes; in extreme instances, legs cross due to increased adductor tone ('scissoring' gait). Upper motor neuron signs present on examination. May be cerebral or spinal in origin. Common causes: cervical spondylotic myelopathy (elderly), demyelinating disease and trauma (younger patients), vascular disease (stroke), multiple sclerosis, motor neuron disease, perinatal injury (cerebral palsy).
4.3 Parkinsonian Gait¶
Affects 1% of population >65 years. Characterized by stooped posture, shuffling gait, and decreased arm swing. Patients sometimes accelerate (festinate) with walking, display retropulsion, or turn en bloc. Falls are a major source of morbidity, particularly later in disease course as balance becomes progressively impaired. Dopamine replacement improves step length, arm swing, turning speed, and gait initiation.
4.4 Freezing of Gait¶
Defined as brief, episodic absence of forward progression of feet despite intention to walk. May be triggered by approaching narrow doorway or crowd; contributes to fall risk. Present in approximately one-quarter of Parkinson's patients within 5 years of onset, frequency increases over time. In patients with motor fluctuations, 'on' state freezing often fails to respond to levodopa changes; auditory and visual cueing strategies may help. End-of-dose freezing may improve with dopaminergic optimization or MAO-B inhibitors (rasagiline, selegiline).
4.5 Atypical Parkinsonian Gaits¶
Freezing is common in PSP, MSA, and corticobasal degeneration. Patients frequently present with axial stiffness, postural instability, and shuffling, freezing gait while lacking characteristic pill-rolling tremor. PSP gait is typically more erect (vs stooped in PD); falls within first year suggest PSP. Vascular parkinsonism tends to be broad-based and shuffling with reduced arm swing bilaterally; disproportionate gait involvement early differentiates from PD.
4.6 Hyperkinetic Movement Disorder Gaits¶
In Huntington's disease, unpredictable choreic movements give gait a dancing quality. Tardive dyskinesia causes stereotypic gait disorders in patients chronically exposed to D2 dopamine receptor blockers. Orthostatic tremor is a high-frequency, low-amplitude tremor predominantly involving lower extremities; patients report shakiness on standing with improvement on sitting or walking; tremor often only appreciable by palpating legs while standing.
4.7 Frontal Gait Disorder¶
Also known as higher-level gait disorder. Common in elderly with variety of causes. Features include wide base of support, short stride, shuffling along floor, and difficulty with starts and turns. Many exhibit 'slipping clutch' syndrome or gait ignition failure. Strength is generally preserved; patients can make stepping movements when not standing and maintaining balance simultaneously. This is a higher-level motor control disorder (not true apraxia).
4.8 Cerebellar Gait Ataxia¶
Characterized by wide base of support, lateral instability of trunk, erratic foot placement, and decompensation of balance when attempting to walk on narrow base. Difficulty maintaining balance when turning is often an early feature. Patients unable to walk tandem heel-to-toe and display truncal sway in narrow-based or tandem stance. Considerable variation in tendency to fall in daily life. Causes: stroke, trauma, tumor, neurodegenerative disease (MSA, hereditary cerebellar degeneration), fragile X premutation (older men), alcohol.
4.9 Sensory Ataxia¶
Classic example is tabetic neurosyphilis. Contemporary equivalent is neuropathy affecting large fibers. Vitamin B12 deficiency is a treatable cause of large-fiber sensory loss. Joint position and vibration sense are diminished in lower limbs. Stance is destabilized by eye closure (Romberg's sign); patients look down at feet when walking and do poorly in dark.
4.10 Neuromuscular Disease Gait¶
With distal weakness (peripheral neuropathy): increased step height to compensate for foot drop, sole may slap on floor during weight acceptance (steppage gait). With proximal weakness (myopathy/muscular dystrophy): excess pelvic sway during locomotion. Lumbar spinal stenosis: stooped posture ameliorates pain from cauda equina compression, may mimic early parkinsonism.
4.11 Other Gait Patterns¶
Dystonia: sustained muscle contractions causing repetitive twisting movements and abnormal posture; may produce plantar flexion and foot inversion, sometimes with trunk torsion; asymmetric dystonia involving gait may signal PD in younger adults. Stiff-person syndrome: exaggerated lumbar lordosis and antagonist muscle overactivation restrict trunk/lower limb movement, resulting in wooden/fixed posture. Toxic/metabolic disorders: mental status changes, asterixis, myoclonus; disequilibrium particularly evident in chronic renal disease and hepatic failure.
4.12 Functional Gait Disorder¶
Key features: sudden onset, inconsistent deficits, waxing/waning course, incongruence with organic lesion, improvement with distraction. Phenomenology is variable: extreme slow motion, inappropriately overcautious gait, gyrations of posture with wastage of muscular energy, astasia-abasia, bouncing, and foot stiffness (dystonia). Falls are rare with discrepancies between examination findings and functional status. Preceding stress/trauma is variably present; absence does not preclude diagnosis.
5. DIFFERENTIAL DIAGNOSIS¶
The differential diagnosis of gait disorders is broad and includes neurologic, orthopedic, and systemic causes. The clinical pattern of gait abnormality, associated neurologic findings, and patient demographics help narrow the differential.
5.1 Neurologic Causes by Pattern¶
Spastic gait: cervical spondylotic myelopathy, MS, stroke, motor neuron disease, cerebral palsy, spinal cord tumor/vascular malformation. Parkinsonian gait: PD, drug-induced parkinsonism, PSP, MSA, corticobasal degeneration, vascular parkinsonism, dementia with Lewy bodies. Cerebellar ataxia: stroke, MS, hereditary ataxias, MSA, alcohol, fragile X premutation. Sensory ataxia: peripheral neuropathy (diabetic, B12 deficiency), tabes dorsalis, autoimmune sensory neuronopathy. Frontal gait: subcortical vascular disease, NPH, neurodegenerative dementias, frontal mass lesions.
5.2 Nonneurologic Causes¶
Orthopedic: osteoarthritis (especially knee, hip), contractures, foot deformities, spinal deformity. Visual impairment. Cardiopulmonary limitations. Deconditioning/generalized weakness.
5.3 Causes of Falls¶
Mechanical/environmental (tripping, slipping). Gait/balance disorder (neurologic causes listed above). Syncope (cardiac arrhythmia, orthostatic hypotension, vasovagal). Seizure. Drop attacks. Medication effects. Cognitive impairment.
6. INVESTIGATIONS & DIAGNOSIS¶
Diagnosis relies primarily on clinical observation and neurologic examination, supplemented by targeted imaging and laboratory testing based on suspected etiology.
6.1 Clinical Gait Assessment¶
Gait observation provides immediate sense of patient's degree of disability. Arthritic and antalgic gaits are recognized by observation. Characteristic patterns of abnormality are sometimes seen, though failing gaits often look similar. Quantifiable measures: cadence (steps per minute), velocity, and stride length can be recorded by timing patient over fixed distance. Timed Up and Go (TUG) test: patient stands from chair, walks 10 feet, turns, and sits down; >12 seconds indicates high fall risk.
6.2 Physical Examination Components¶
Cardiac: rhythm irregularities, murmurs. Orthostatic vitals: compare supine to standing pressures (immediately and at 3 minutes); significant if systolic drop >20 mmHg, diastolic drop >10 mmHg, or marked heart rate increase. Visual acuity with typical eyewear; peripheral fields if visual field cut suspected. Hearing assessment if vestibular problem suspected. Standing posture: spinal deformity (kyphosis, lordosis, scoliosis). Lower extremities: knee alignment, ankle/hindfoot pronation. Feet: calluses, hallux valgus, hammertoes, arch loss. Footwear: fit, heel attachment, tread depth, wear pattern.
6.3 Neurologic Examination¶
Mental status: assess while obtaining history. Motor examination: hip abductors/flexors, knee extensors/flexors, ankle dorsiflexors/plantar flexors. Tone assessment when neuromuscular disease suspected. Sensory examination: monofilament testing for neuropathy. Romberg test for sensory ataxia. Cerebellar signs (heel-to-shin, tandem gait). Upper motor neuron signs for spastic gait.
6.4 Imaging Studies¶
MRI brain: sensitive for vascular or demyelinating cerebral lesions; good screening for occult hydrocephalus. Findings in NPH: ventricular enlargement, enlarged flow void about aqueduct, periventricular white matter change, high-convexity tightness (disproportionate widening of sylvian fissures versus cortical sulci). Patients with recurrent falls: screen for subdural hematoma. Many elderly patients have periventricular/centrum semiovale white matter abnormalities; substantial burden impacts cerebral control of locomotion. MRI spine for suspected myelopathy. MRI cerebellum: demonstrates extent and topography of cerebellar atrophy.
6.5 Laboratory Testing¶
Vitamin B12 level for suspected sensory ataxia/myelopathy. Vestibular function testing when vestibular deficit suspected. Lumbar puncture or dynamic test necessary to confirm NPH diagnosis. Additional testing based on suspected etiology (e.g., paraneoplastic antibodies for subacute sensory neuronopathy).
6.6 Quantitative Gait Analysis¶
Standard in research settings; potential to inform diagnosis and treatment when more widely adopted clinically. Devices include instrumented walkways, motion capture systems, and wearables.
7. MANAGEMENT & TREATMENT¶
Treatment is directed at the underlying cause of gait disorder when possible, combined with rehabilitation strategies, fall prevention measures, and appropriate assistive devices.
7.1 Parkinsonian Gait Treatment¶
Dopamine replacement improves step length, arm swing, turning speed, and gait initiation. For end-of-dose gait freezing: optimize dopaminergic drugs or use MAO-B inhibitors (rasagiline, selegiline). For 'on' state freezing (often fails to respond to levodopa changes): auditory and visual cueing strategies. Cholinesterase inhibitors (donepezil, rivastigmine) may decrease fall frequency even without cognitive impairment, perhaps through attention improvement. Evidence suggests cholinergic circuit deficits in pedunculopontine nucleus and cortex contribute to PD gait disorder.
7.2 Spastic Gait Treatment¶
Treat underlying cause when possible. Myelopathy: exclude structural lesion (tumor, vascular malformation) with appropriate testing. Cervical spondylosis: surgical decompression may be indicated. MS: disease-modifying therapy. Symptomatic management of spasticity (baclofen, tizanidine, botulinum toxin).
7.3 Cerebellar Ataxia Treatment¶
Treatment depends on etiology. Alcohol cessation for alcohol-related cerebellar degeneration. Physical therapy for balance and coordination training. Progression often measured by years to loss of stable ambulation.
7.4 Sensory Ataxia Treatment¶
Vitamin B12 replacement for deficiency. Treat underlying neuropathy when possible. Compensatory strategies: good lighting, visual monitoring during ambulation.
7.5 Frontal Gait Disorder Treatment¶
For vascular etiology: vascular risk factor modification. For NPH: lumbar puncture or dynamic test to confirm diagnosis; ventriculoperitoneal shunting may improve gait. Differentiate from neurodegenerative dementias and frontal mass lesions by neuroimaging.
7.6 Cautious Gait Treatment¶
Physical therapy often improves walking. Address fear of falling. Follow-up observation may reveal more specific underlying disorder.
7.7 Toxic/Metabolic Disorder Treatment¶
These disorders are especially important to recognize because they are often treatable. Medication review and adjustment: sedative drugs (especially neuroleptics, long-acting benzodiazepines) affect postural control and increase fall risk. Treat underlying metabolic derangement (uremia, hepatic failure).
7.8 Rehabilitation and Physical Therapy¶
Essential component of management for most gait disorders. Balance training, strength training, gait retraining. Compensatory strategies for sensory deficits.
7.9 Assistive Devices¶
By age 80, one in four uses mechanical aid for ambulation. Canes, walkers as appropriate to level of disability. Proper fitting essential.
8. FALLS: ASSESSMENT AND PREVENTION¶
Falls represent a major source of morbidity in the elderly. A systematic approach to assessment and multifactorial intervention can reduce fall risk.
Common Risk Factors for Falls in Older Adults¶
| Risk Factor | Details |
|---|---|
| History of falls | Strong predictor of future falls |
| Gait and/or balance disorder | Neurologic and nonneurologic causes |
| Visual deficits | Impairs environmental awareness |
| Physical disability | Includes muscle weakness, use of assistive devices, osteoarthritis of the knee |
| Orthostatic hypotension | Systolic drop >20 mmHg or diastolic drop >10 mmHg on standing |
| Depression | Associated with inactivity and psychomotor changes |
| Cognitive impairment | Impairs attention and executive function |
| Risk Factor | Details |
|---|---|
| Medications | Polypharmacy, antipsychotics, antidepressants, benzodiazepines, anticholinergics, antihypertensives, diuretics |
8.1 Screening Recommendations¶
All community-dwelling adults should be asked annually about falls and whether fear of falling limits daily activities. Patients with history of falls or TUG >12 seconds are at high risk and should undergo further assessment.
8.2 History Taking for Falls¶
History is often problematic or incomplete; underlying mechanism may be difficult to establish in retrospect. Attentive observer report can be invaluable. Key questions: sudden drop without provocation (suggests syncope, seizure, or other neurologic event); gait freezing/festination (suggests parkinsonism); falling after arising from chair or minor perturbation (suggests muscular strength issue); falls in changing footing situations or poor lighting (suggests sensory deficits). Elicit provoking factors (head turn, standing, carrying object) and prodromal symptoms (dizziness, vertigo, presyncope, focal weakness). Establish baseline mobility and medical comorbidities.
8.3 Medication Review¶
Particularly important to review: benzodiazepines, opioids, antipsychotics, antiepileptics, antidepressants, antiarrhythmics, diuretics, antihypertensives, anticholinergics. Polypharmacy ( ≥ 4 prescription medications) is an independent risk factor.
8.4 Distinguishing Fall Types¶
Important to distinguish mechanical falls (tripping, slipping due to purely extrinsic/environmental factors) from those with possibly modifiable intrinsic factors. Recurrent falls suggest underlying gait or balance disorder. Falls with loss of consciousness (syncope, seizure) may require cardiac or neurologic evaluation; patient report of consciousness change may be unreliable.
8.5 Consequences of Falls¶
Hip fractures: hospitalization, nursing home admission risk, substantially increased mortality in subsequent year. Brain or spinal injury: history may be difficult to obtain. Prolonged time lying on ground: risk for dehydration and rhabdomyolysis. Subdural hematoma in recurrent fallers. Fear of falling leads to activity restriction in nearly one in five elderly.
9. DISORDERS OF BALANCE¶
Balance is the ability to maintain equilibrium—a dynamic state in which the center of mass is controlled with respect to lower extremities, gravity, and support surface despite external perturbations.
9.1 Neuroanatomy of Balance¶
Balance reflexes require input from cerebellar, vestibular, and somatosensory systems. Output is mediated by premotor cortex and corticospinal and reticulospinal tracts to axial and proximal limb muscles. These responses are physiologically complex with incompletely understood anatomic representation.
9.2 Cerebellar Imbalance¶
Patients with cerebellar ataxia do not generally complain of dizziness, although balance is visibly impaired. Neurologic examination reveals variety of cerebellar signs. Postural compensation may prevent falls early, but falls are inevitable with disease progression. Progression of neurodegenerative ataxia often measured by years to loss of stable ambulation.
9.3 Vestibular Disorders¶
Symptoms and signs fall into three categories: (1) vertigo (subjective inappropriate perception or illusion of movement); (2) nystagmus (involuntary eye movements); (3) impaired standing balance. Not every patient has all manifestations. Patients with ototoxic drug-related vestibular deficits may lack vertigo or obvious nystagmus, but balance is impaired on standing/walking and they cannot navigate in dark. Laboratory testing available to investigate vestibular deficits.
9.4 Somatosensory Imbalance¶
Produces imbalance and falls with subjective sense of insecure balance and fear of falling. Postural control compromised by eye closure (Romberg's sign); difficulty navigating in dark. Dramatic example: autoimmune subacute sensory neuronopathy (sometimes paraneoplastic). Compensatory strategies enable walking in virtual absence of proprioception, but task requires active visual monitoring.
9.5 Higher-Level Equilibrium Disorders¶
Patients have difficulty maintaining balance in daily life and may present with falls. Awareness of balance impairment may be reduced. Patients taking sedating medications are in this category.
10. KEY POINTS & CLINICAL PEARLS¶
Essential concepts for clinical practice in the evaluation and management of gait disorders, imbalance, and falls.
Clinical Pearls for Gait Disorders and Falls¶
| Topic | Key Point |
|---|---|
| Prevalence | 15% affected at age >65; 40% at age ‡85; one in four uses assistive device by age 80 |
| Sensory requirements | Loss of 2 of 3 sensory systems (visual, vestibular, proprioceptive) compromises balance |
| Most common neurologic gait disorder | Sensory ataxic gait (18%), usually due to peripheral sensory neuropathy |
| Cautious gait | Nonspecific adaptation to perceived postural threat; present in >1/3 of elderly with gait impairment |
| Freezing of gait in PD | Present in ~25% within 5 years of onset; may respond to cueing strategies or MAO-B inhibitors |
| Frontal gait disorder | Most commonly due to subcortical small-vessel vascular disease; consider NPH if triad present |
| NPH imaging clues | Ventricular enlargement, enlarged aqueductal flow void, periventricular white matter change, high-convexity tightness |
| Vitamin B12 deficiency | Treatable cause of large-fiber sensory loss in spinal cord and peripheral nervous system |
| TUG test | >12 seconds indicates high fall risk requiring further assessment |
| Topic | Key Point |
|---|---|
| Orthostatic hypotension criteria | Systolic drop >20 mmHg OR diastolic drop >10 mmHg OR marked HR increase |
| Dual-task walking | Ability to walk while attending to cognitive task may be compromised in elderly; decline associated with dementia risk |
| Functional gait disorder clues | Sudden onset, inconsistent deficits, improvement with distraction, falls are rare |
| Cholinesterase inhibitors in PD | May reduce falls even without cognitive impairment through attention improvement |
| Annual screening | All community-dwelling adults should be asked about falls and fear of falling limiting activities |
| Polypharmacy | ‡4 medications is independent risk factor for falls; review and reduce when possible |