Balance and gait disorders

Deema Fattal MD (Dr. Fattal, Director of the Balance Disorders Clinic at the University of Iowa, has no relevant financial relationships to disclose.)
Douglas J Lanska MD FAAN MS MSPH, editor. (

Dr. Lanska of the University of Wisconsin School of Medicine and Public Health, the Medical College of Wisconsin, and IM Sechenov First Moscow State Medical University has no relevant financial relationships to disclose.

Originally released September 16, 2003; last updated December 15, 2014; expires December 15, 2017
Notice: This article has expired and is therefore not available for CME credit.

This article includes discussion of balance and gait disorders, gait disturbances, gait failure, and walking disorders. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.


Human walking is unique, and each of us has a “fingerprint” (or footprint) walk unlike any other. Bipedal walking is almost strictly a human skill. The evolution of bipedalism over the last 6 million years helped free the hands and possibly paved the way toward tool development and the eventual evolution of modern humans. Walking is not an aimless endeavor—it is essential for survival. For this reason, balance and gait disorders have serious consequences to the afflicted. In this updated article, the author delineates how the topic of balance and gait continues to grow. For example, the new term motoric cognitive risk has been coined to delineate a group of elderly who have slow gait and subjective cognitive complaints. Such patients are at increased risk of developing dementia. We all slow down with age, but elderly who slow by more than 1 cm/s/year have an increased risk of dementia. Furthermore, there is a strong interaction among these factors: gait speed, white matter disease, cerebrovascular disease, dementia, and depression, all important to evaluate while screening patients. In the clinic (as in research), a change in gait speed of 10 cm/s seems clinically meaningful. On the basic science level, researchers found that arm swing is not passive but active, and that the number of steps needed to turn is stable (which is an important clinical tool). Texting while walking can be hazardous even in the young. Finally, advanced gait analysis methods can differentiate premanifest Huntington patients from controls, whereas basic gait testing does not.

Historical note and terminology

Human walking is unique, and each of us has a “fingerprint” (or footprint) walk unlike any other. Bipedal walking is almost strictly a human skill. The evolution of bipedalism occurred after the chimpanzee-human diversion about 6 million years ago and it evolved over a few million years so that by the time of the skeleton “Lucy” (3.2 million years ago), she was mostly upright, and by 2 million years ago, our ancestors became obligate bipeds. Bipedalism helped free the hands and possibly paved the way towards tool development and the eventual evolution of modern humans (Nielsen 2003). Currently, we all still belong to 1 species, with our skeletons staying similar over the last 200,000 years, yet evolution is ongoing; for example, blue eyes evolved only few thousand years ago.

Balance is the ability to stand up and remain upright against the force of gravity (equilibrium), and gait is rhythmic stepping movements to advance in space (locomotion). All vertebrates, including humans, have a desired body orientation that they maintain (in animals it is dorsal side up, and in humans it is upright posture) (Grillner et al 2008). Balance and gait abilities in man depend on a hierarchal system of muscles, nerves, and interconnected central nervous system structures that is amazingly similar to that seen all the way “down” to the snail (Orlovsky et al 1999). Walking is not an aimless process and is essential for survival of animal and human. For this reason, disorders of balance and gait have serious consequences to the afflicted. Because such disorders almost always coexist, they are discussed together, under the rubric of “balance and gait disorders.”

An excellent summary of the history of gait disorder was provided by Clarac in 2008 (Clarac 2008). The first scientific description of human locomotion was undertaken by Borelli in 1680, where he analyzed joint movements and forces. In the 18th century, Johann Unzer demonstrated that spinalized birds and mammals could walk nearly normally. The 19th century witnessed the birth of modern medicine, with the advent of systematic description of illnesses (with Charcot studying locomotor ataxia, Romberg describing the now called Romberg sign, Duchenne electrically stimulating muscle, and German neurosurgeons Gustav Fritsch and Eduard Hitzig directly stimulating the cortex and eliciting movement). The prevailing concept then was that movement is centrally mediated. But Charcot argued that locomotor centers resided in both the cerebral cortex and spinal cord. In 1910, Sherrington also described a “rhythm-generating role for the spinal cord” based on different animal preparations (intact, decerebrate, spinal). Graham Brown also worked on animal preparations and proposed the concept of “half centers” in the spinal cord in 1914. The concept of a spinal central pattern generator, though, did not get solidified until the 1960s (with the publication of 2 seminal works of reduced animal preparations by Cornelius Wiersma and Donald Wilson). Then, in the 1960s and 1970s, the Russian neuroscientists Maurice Shik and Grigori Orlovsky used precollicular cat preparations and found the midbrain locomotor region that we now know exists in all vertebrates (Shik et al 1966). Sten Grillner and his group worked on decerebrate and deafferentated animals and confirmed the presence of complex movements even in after deafferentation, demonstrating the dynamicity of the central pattern generator activity.

The systematic study, documentation, and categorization of balance and gait disorders were facilitated by the widespread advent of photography and cinematography during the 20th century, pioneered by ingenious work by Muybridge and Marey (Dercum 1888; Muybridge 1899; Cantacuzene 1973; Aubert 2000; Lanska and Goetz 2000; Lanska 2001; Goetz 2002; Clarac 2008). Marey gave his walking and trotting dog pictures to Maurice Philippson who described the “step cycle” in 1905 (Clarac 2008). Baker provides an interesting review of gait analysis techniques (Baker 2007).

Despite advances over the last century in classifications of balance and gait disorders due to peripheral nervous system, spinal cord, cerebellum, thalamic, and basal ganglia diseases, balance and gait disorders due to cerebral (cortical or subcortical white matter) lesions remain elusive to clear and distinct classifications. For example, late in the 19th century, Bruns coined the term frontal ataxia to describe cerebral-related (mainly frontal lobe) balance and gait disorders, but his term fell out of favor; the concept of frontal gait apraxia began to be used during the first quarter of the 20th century and continues to be used, with some controversy, into the 21st century. Gerstmann and Schilder in 1926 described 2 patients with frontal lesions who were unable to lift feet to walk and could not stand or sit without falling backwards; they called it gait apraxia (Thompson 2012). In 1960, Meyer and Barron reviewed frontal lobe and gait cases; they emphasized the presence of slow, wide, short shuffling steps, freezing, reduced step height, retropulsion, abnormal abstract leg movements, perseveration, rigidity, hypokinesia, and the lack of dysmetria or dysarthria or nystagmus--all features making “frontal ataxia” different from cerebellar ataxia (Thompson 2012). Over the last 100 years, in addition to gait apraxia and frontal ataxia, many other terms attributed to cerebral balance and gait disorders have been proposed, adding to the confusion. Table 1 is a non-exhaustive list of the plethora of overlapping terminology used to describe cerebral balance and gait disorders over the last century (Koller et al 1983; Thompson and Marsden 1987; Winikates and Jankovic 1999; Jankovic et al 2001; Nutt 2001; Thompson 2001; Della Sala et al 2002; Baezner and Hennerici 2005; Elble 2007; Thompson and Nutt 2007). More terms and older literature are reviewed by Della Sala and colleagues (Della Sala et al 2002).

Despite the confusing terminology surrounding cerebral balance and gait disorders, and despite our limited understanding of their pathophysiology, historical cases show that cerebral balance and gait disorders are caused by mainly frontal and occasionally parietal lesions (Van Bogaert and Martin 1929; Frazier 1936; Della Sala et al 2002) and that cerebral balance and gait disorders are characterized by varying combinations of parkinsonian, ataxic, spastic, “magnetic” (feet stuck to ground), and “apractic” qualities.

For simplification, this article adopts a generic term, cerebral balance and gait disorders, to refer to balance and gait disorders due to cortical or subcortical lesions.

Table 1. Nomenclature of Cerebral (Essentially Frontal) Balance and Gait Disorders Over the Last Century

Disorder name


• Melokinetic apraxia
• Frontal ataxia (frontale ataxie)
• Binswanger disease
• Trepidante abasie (trepidant abasia)
• Marche a petits pas
• Remarkable clumsiness (eingentümliche
• Corticale apraxie
• Loss of the technical requirements of the movements
(bewegungstechnische schwierigkeit)
• Innervatory apraxia (innervatorische apraxie)
Limb-kinetic apraxia (gliedkinetische apraxie)
• Bilaterale motorische apraxie
• Gawky movements (tapsigkeit)
• Motorische apraxie
• Gait apraxia
• Trunk apraxia (torso apraxie)
• Frontal disequilibrium (déséquilibration frontale)
• Arteriosclerotic parkinsonism
• Senile gait
• Unbeholfenheit (awkwardness)
• Apraxia
• Petren gait
• Magnetic foot response
• Magnetic apraxia
• Repellent apraxia
• Trunk apraxia
• Slipping clutch syndrome
• Gait apraxia
• Apraxia
• Pure akinesia
• Axial apraxia
• Akinetic parkinsonism
• Lower half parkinsonism
• Parkinsonian-ataxia
• Lower body parkinsonism
• Hypersensitivity braking
• Primary progressive freezing gait
• Gait ignition failure
• Higher level gait disorder
- Subcortical disequilibrium
- Subcortical gait disorders
- Frontal gait disorders
• Nonspecific disequilibrium of elderly
• Higher level gait disorder
• Vascular parkinsonism
• Frontal lobe gait disorder
• Gait apraxia-term revisited
• Higher level gait disorder:
(i) ignition apraxia
(ii) equilibrium apraxia
(iii) mixed apraxia
• Vascular higher-level gait disorders
• Psychomotor disadaptation syndrome
• Elderly with cautious gait of unknown origin
• Senile paraplegia
• Parkinsonian ataxia
• Mild parkinsonian signs concept
• Higher level gait disorder
• High-level gait disorder

(Nothnagel 1879)
(Bruns 1892)
(Binswanger 1894)
(Petren 1901)
(Marie 1901)
(Liepmann 1905)

(Heilbronner 1905)
(Kleist 1907)

(Kleist 1907)
(Westphal 1907)
(Bonhoffer 1914; von Monakow 1914)
(Poppelreuter 1917)
(Liepmann 1920)
(Gerstmann and Schilder 1926)
(Sittig 1929)
(Van Bogaert and Martin 1929)
(Critchley 1929)
(Critchley 1931; Koller et al 1985)
(Kleist 1934)
(Bell 1934)
(Critchley 1948)
(Denny-Brown 1958)
(Denny-Brown 1958)
(Denny-Brown 1958)
(Denny-Brown 1958)
(Denny-Brown 1958)
(Meyer and Barron 1960)
(Petrovici 1968)
(Imai and Narabayashi 1974)
(Lakke 1985)
(FitzGerald and Jankovic 1989)
(Thompson and Marsden 1987)
(Thompson and Marsden 1987)
(FitzGerald and Jankovic 1989)
(Mestre et al 1992)
(Achiron et al 1993)
(Atchison et al 1993)
(Nutt et al 1993)

(Fife and Baloh 1993)
(Tyrrell 1994)
(Zijlmans et al 1995)
(Thompson 2001)
(Della Sala et al 2002)
(Liston et al 2003)

(Martin and O'Neill 2004)
(Mourey et al 2004)
(Giladi et al 2005)
(Thompson 2007)
(Thompson 2007)
(Louis and Bennett 2007)
(Huber-Mahlin et al 2010)
(Kafri et al 2013)

In the realm of “non-organic” balance and gait disorders, Jaccoud described in 1860 the inability to stand (astasia) or walk (abasia) in the face of normal limb movement (Keane 1989; Thompson 2001). Later, S Weir Mitchell described similar patients, and in 1880 Charcot's work popularized hysteria (Keane 1989; Goetz 2002). The term astasia-abasia was first used by Paul Blocq in his seminal work in 1888 and soon came to mean “non-organic” gaits (Okun and Koehler 2007); such use of the term astasia-abasia, however, is not precise and should be discouraged. Therefore, the terms psychiatric balance and gait disorders (referring to psychiatric ailments, such as schizophrenia or depression) or psychogenic balance and gait disorders (referring to balance and gait disorders due to somatoform disorder, eg, “conversion disorder” when a known stress is present or “somatoform disorder not otherwise specified” when no known stressful event is present) should be utilized instead (American Psychiatric Association 2000). Please note that “conversion disorder” and “somatoform disorder not otherwise specified” diagnoses can loosely be used interchangeably.

The content you are trying to view is available only to logged in, current MedLink Neurology subscribers.

If you are a subscriber, please log in.

If you are a former subscriber or have registered before, please log in first and then click select a Service Plan or contact Subscriber Services. Site license users, click the Site License Acces link on the Homepage at an authorized computer.

If you have never registered before, click Learn More about MedLink Neurology  or view available Service Plans.