A. Importance of the station and gait examination
If we had just one chance to make the diagnosis, we would choose the most important single part of the neurologic examination: watching the Pt rise, stand, and walk. First notice how the Pt rises and the steadiness of the vertical posture. Then ask the Pt to walk freely back and forth. As the Pt walks, look for irregular strides, lack of a heel-to-toe foot action, unsteadiness, a wide-based gait, an overplay of involuntary movements, and lack of or excessive arm swinging. Notice whether the Pt turns by stepping around freely or rotates on the spot, en bloc, with tiny steps (see parkinsonian gait and marche à petit pas, below). Next, test triceps surae strength and balance by having the Pt walk on the balls of the feet and then on the heels. Next request tandem walking (heel-to-toe down a straight line). Finally, request a deep kneebend. Ask a child to run and hop. Throughout, note how well the Pt comprehends and executes the commands. Retarded, demented, psychotic, and passive-aggressive or oppositional Pts require constant coaxing.
If the Pt rises, stands, and walks completely normally, then, in all probability, the Pt's motor system is completely intact. If the Pt's motor system is completely intact, then, in all probability, the sensory system is completely intact. If the Pt follows all commands promptly and well, with no confusion or hesitancy, then in all probability the Pt's mental state and sensorium are intact. With motor, sensory, and mental functions intact, then, in all probability, the Pt's nervous system is intact. Of course, you must still complete the entire neurologic examination to confirm these initial inferences. A normal gait requires the integrity of vast circuits of the peripheral and central nervous systems: circuits that underlie the willing of movements and the antigravity, supporting, and righting reflexes; circuits that coordinate the rate, regularity, and force of the muscular contractions; circuits that generate reciprocal limb actions; and circuits that mediate touch, proprioception, and vision. Most disorders of the muscles, nerves, spinal cord, cerebellum, brainstem, basal ganglia, or cerebrum impair the gait and in a characteristic way. Thus, the features of the gait disorder suggest the lesion location and probable cause.
Gait examination begins with the genetically preprogrammed automatic or reflex stepping of the neonate. If the Ex holds the neonate vertically, with its feet contacting the bed surface, the infant reflexly lifts its legs alternately and steps. Voluntary trunk control and voluntary standing will later replace automatic stepping, leading to a cruising gait, in which the infant takes steps when holding onto a couch or when steadied by a parent. Then, at about 1 year the infant walks freely, with a toddler's gait, featured by a broad-base, short, jerky, irregular steps, a semiflexed posture of the arms, and frequent falls (progression by three steps and a plop). After the toddler stage the child develops a normal mature gait, with a narrow-based, heel-toe stride, contrabody movement, and reciprocal swinging of the arms (Woollacott et al., 1989). The gait sequence merely reflects a general law of infant development, that inborn, so-called primitive reflexes or behaviors predate all voluntary actions. Thus, smiling, chewing, sucking, grasping, breathing, and walking occur reflexly before the brain and its pathways mature to control these actions voluntarily.
Let us start with the neuromuscular system and work up to cerebral lesions. If you wish to learn the most from this essay, I strongly recommend that you get up and act out the gaits described. First get up and imitate the toddler gait. If an infant has a club-foot gait, the gait depends on which of a variety of valgus or varus deformities exists. With tibial torsion, the infant has an in-toed or pigeon-toed gait. Many clubfoot deformities correct themselves. Most myopathies (the muscular dystrophies and the polymyositises) weaken the proximal muscles of the shoulders, back, and hips. Because of weak paraspinal muscles, the myopathic Pt shows a characteristic, usually sway-backed, waddle, a lordotic waddling gait resembling the pride of pregnancy gait of the third trimester. Because of the weak proximal muscles, the myopathic Pt has trouble when getting up on or down from the examining table or when standing up from a sitting or especially a reclining position. In so arising, the myopathic Pt may display Gower's sign, the bracing of the arms against the thighs to push the weak trunk erect.
This 4-year-old boy, striding on the balls of his feet, without a definite heel strike has a toe-walking gait (Sala et al., 1999). Tight heel cords limit dorsiflexion of the foot to about 90 degrees. Such a gait occurs in Duchenne's muscular dystrophy, in spastic diplegia, and in autistic or other retarded children. But the next toe-walking child moves along jauntily, runs, skips, and hops normally and has none of these serious disorders, merely an idiosyncratic, sometimes familial, gait pattern.
The next Pt's toes do not clear the floor because of paralysis of foot dorsiflexion, causing a toe-drop or foot-drop gait. In compensation, the Pt jerks the knee high, flipping the foot up into dorsiflexion, and slaps the foot down. With unilateral or bilateral foot-drop gait, the sound of the slapping feet alone permits the Ex to suspect the diagnosis, without even seeing the Pt. Unilateral foot drop suggests a unilateral, perhaps mechanical or compressive, neuropathy of the common peroneal nerve, frequently from a crossed-knee palsy. A bilateral foot-drop or steppage gait suggests a symmetrical distal peripheral neuropathy of toxic, metabolic, or heredofamilial type, as in alcoholic neuropathy or Charcot-Marie-Tooth progressive peroneal atrophy.
A tibial nerve palsy, in contrast to a peroneal nerve palsy, causes a heel-drop gait. The Pt can dorsiflex the foot but not plantar flex it. A complete sciatic palsy causes a flail-foot gait in which the Pt can neither dorsiflex nor plantar flex the foot. Now you see why the Ex asks the Pt to walk on the toes and the heels. These actions test all the muscles innervated by the sciatic nerve, in addition to proprioception and balance.
A tabetic, dorsal column, or sensory ataxic gait resembles a double foot-drop or step-page gait but has its own unique signature. In tabes dorsalis, syphilitic infection causes degeneration of dorsal roots and dorsal columns of the spinal cord. Lacking position sense, the Pt lifts the knees too high and slaps the feet down, placing them irregularly and on a broad base, because of sensory ataxia. The Pt simply does not know where the legs are. When in bed, the Pt literally has to peek under the covers to locate the feet and legs. To compensate for the lack of position sense, the tabetic Pt must use visual cues to stand. Eye closure removes the visual cues that compensate for the absence of position sense. The Pt then sways and falls over, thus failing the Romberg test (Chapter 10), which the cerebellar Pt more or less passes. The steppage gait of dorsal column disease differs from the double foot-drop gait of peroneal palsy by the presence of normal dorsiflexor power, irregular foot placement due to the sensory ataxia, the absence of position and vibration sense in the legs, absence of MSRs, and abnormal Romberg test. The presence of Argyll Robertson pupils and a positive serologic test for syphilis (Table 4-5) separates tabes dorsalis from other dorsal column diseases such as the subacute combined degeneration of pernicious anemia or the spinocerebellar degenerations. The experienced Ex will not confuse any of the gaits in this entire essay with the slow, deliberate, searching steps of the blind Pt, the blind person's gait.
The next Pt has a painful sole or hyperesthetic gait. The Pt sets the foot down gingerly, bears as little weight on it as possible, and limps off the foot as soon as possible while wincing and hunching the shoulders. This feature, the limiting of weight bearing by pain, is the antalgic gait. If the pain is unilateral and on the bottom of the ball of the foot, suspect Morton's metatarsalgia, a painful neuroma of an interdigital nerve; if it affects the large toe (podagra), consider gout. If the pain is bilateral, the Pt looks like a person walking barefoot on a hot pavement; suspect hyperesthesia of both soles, common in painful distal peripheral neuropathies, usually metabolic, toxic, or alcoholic or nutritional in origin. When the Pt complains of foot pain, always examine the Pt's shoes—the wear pattern tells a tale in itself—and compare the size and shape of the shoe with the size and shape of the foot and note the heel height.
The next Pt has a radicular or back pain posture and an antalgic gait. The Pt complains of extreme pain radiating into the big toe, caused, in all probability, by a herniated intervertebral disc compressing the L5 nerve root. Coughing, or straight-leg raising causes shooting pain into the foot (pp. 399–404). To rise from a chair, the Pt pushes up with the arms and has a stiff back, with a completely flat lumbar curve. When standing, the Pt does not put weight on the painful leg and gets off of it as soon as possible (antalgic gait). The Achilles tendon feels soft to compression by the Ex's thumb, as compared with the weight-bearing leg. When walking, the Pt places little weight on the painful leg and takes stiff, slow, short strides with no heel strike, to avoid painful jarring. Often the Pt's trunk tilts slightly to the side opposite the pain.
Even upper extremity neuropathies may cause a characteristic gait disorder. If the Pt's transverse carpal ligament compresses the median nerve, causing a carpal tunnel syndrome, excruciating pain in the hand typically awakens the Pt at night. Night after night, the Pt gets up and paces the bedroom flipping or shaking the hand in an effort to gain some relief, the nocturnal flipping-hand gait, a nearly pathognomonic gait. Autistic and other retarded children show a variety of flipping-hand gaits as repetitive, self-stimulating mannerisms.
E. Cerebellar ataxic gaits
Cerebellar lesions cause dystaxia of voluntary movements and of voluntarily maintained postures, hence, a reeling stance and gait. A unilateral cerebellar lesion causes only ipsilateral cerebellar signs, most likely from neoplasm, infarct, or demyelinating disease. After an acute cerebellar lesion, the Pt frequently veers or falls in one direction (lateropulsion, anteropulsion, or retropulsion). Bilateral cerebellar signs, thus a pancerebellar syndrome, imply a toxic, metabolic, or heredofamilial disorder or multiple sclerosis, if combined with other exacerbating and remitting signs. Relatively pure dystaxia of the legs and gait, with little or no dystaxia of the arms, and no dysarthria or nystagmus suggest a rostral vermis syndrome, most commonly secondary to alcoholism. The painful peripheral neuropathy of such Pts also may cause an antalgic gait. Relatively pure truncal ataxia suggests a flocculonodular lobe or a caudal vermis lesion, generally a tumor (Bastain et al., 1998; Table 8-3).
With a hemiplegic gait, the Pt circumducts a leg, dragging the toe, placing the ball down without a heel strike, with the ipsilateral arm held in partial flexion or, more rarely, flaccidly at the side. Hemiplegia affects the hand and arm more than the leg and usually causes a closed fist because of flexor spasticity. The lesion is most likely an infarct, tumor, or trauma. The next Pt walks with stiff legs, not clearing the floor with either foot, the exact opposite of the Pt with a high steppage gait. This Pt gives the appearance of wading through water because she must work against the spastic opposition of her own muscles, as if walking in a viscid environment of molasses instead of air. Her knees tend to rub together in a scissoring action. She has a spastic gait. If the Pt has a spastic diplegic gait from cerebral palsy, she has small, short legs in contrast to normally developed chest, shoulders, and arms. In spastic diplegia, in direct contrast to double hemiplegia, the Pt has severe spasticity in her legs, minimal spasticity in her arms, and little or no deficit in speaking or swallowing (Gage, 1992), whereas the double hemiplegic has pseudobulbar palsy and the arm is weaker than the leg. The cerebral palsy Pt may adduct the legs strongly when walking, causing a scissors gait. The knees of some spastic diplegics may remain bent when walking, the spastic diplegic crouch gait (Tylkowski and Howell, 1991). The Pt looks as if wading through water or molasses with the knees bent. A pure spastic or paraplegic gait, with no sensory deficits, coming on after infancy, suggests a pure corticospinal tract disorder, such as familial spastic paraplegia. If, in addition to spasticity, the disease impairs the dorsal columns or cerebellum, the Pt will have a wider-based unsteady gait and take irregular steps—the spastic-ataxic gait, suggesting a spinocerebellar degeneration or multiple sclerosis.
G. Basal motor nuclei gaits
When the Pt with a choreiform gait walks, the play of finger and arm movements increases or may even appear clearly for the first time. Random missteps mar the evenness of the strides as the choreiform twitches supervene. Station is characteristically broadbased. A family history of chorea and dementia establishes Huntington's chorea. A history of rheumatic fever, the acute onset of chorea, and a fussy personality signify Sydenham's chorea. When the athetoid Pt walks, the slow writhing movements of fingers and arms tend to increase. A combination of athetosis with moderate spastic diplegia or double hemiplegia, a spastic-athetoid gait, usually signifies status marmoratus (état marbre) of the basal ganglia and thalamus, secondary to perinatal hypoxia. The Pt's great toe may automatically extend when walking, a so-called striatal toe.
Dystonia may first manifest in a child, say of 9 years of age, by an intermittent in-turning of one foot that impedes walking, a dystonic equinovarus gait. In the later stages, dystonic truncal contortions and tortipelvis may cause the trunk to incline strongly forward. The Pt may take giant uneven strides, exhibiting flexions or rise and fall of the trunk, the dystonic dromedary gait, imitating the ungainly gait of a dromedary camel. It looks for all of the world like histrionics, but the Pt has dystonia musculorum deformans, an organic, hereditary disorder. Genetic screening for the DYT gene abnormalities may be useful for patients with early onset dystonia or those with affected relatives. Patients with involuntary movement disorders can sometimes walk backward or dance better than they can walk forward.
This next Pt, with a parkinsonian gait, has a tremor at rest that disappears during voluntary movement, a flexed posture, rises and walks slowly with short steps, lacks any arm swing, and turns en bloc like a statue rotating on a pedestal. The Pt does not have a wide-based gait, as in cerebellar disease. If the Ex (after a warning) shoves the parkinsonian Pt, the Pt will move forward or backward on tiny steps of increasing speed and decreasing length, as if chasing the center of gravity, and may fall over, a festinating gait. Patients with the marche à petit pas often also turn en bloc and festinate. Parkinsonism results from degeneration of the substantia nigra or from neuroleptic medication. Primary progressive freezing gait belongs in the Parkinson category but does not respond to levodopa. The Pts freeze when starting to walk and when turning or in response to some stimulus. They show bradykinesia and a masked face. They get progressively worse, begin to fall, exhibit retropulsion, and become wheelchair dependent in about 4 to 5 years (Factor et al., 2002).
Gait abnormalities often precede dementia of any type (Verghese et al., 2002). This elderly Pt with the shuffling, short steps, who does not lift the feet far from the floor, has the marche à petit pas (the march of small steps; Masdeu et al., 1997; Nutt et al., 1993; Sudarsky, 1990). When the Pt tries to speak, steps cease, leading to the somewhat pejorative, but expressive, colloquialism: "He can't walk and chew gum [in this case walk and talk] at the same time." The aged or demented brain loses the capacity for "dual-tasking" (Haggard et al. 2000). Many of the elderly Pts in a nursing home display this type of gait. It may result from senility (Masdeu et al., 1997), Alzheimer's disease, multi-infarct dementia, or periventricular lesions on MRI (Benson et al., 2002; Whitman et al., 2001).
A glance around a nursing home will disclose many Pts with forward flexion of the head, head drop or head ptosis. Many times the Pt has lost the sense of verticality: the entire trunk tilts in the chair, and the Pt goes to sleep in the head-dropped, body-tilted posture. The posture may result from neuromuscular disorders that cause weakness of the neck muscles, but it often coexists with dementia, parkinsonism, a forward flexed posture of the entire spine, called camptocormia (Umpathi et al., 2002), and usually a disorder of gait.
The next Pt, an elderly woman, has difficulty initiating the sequence of movements to rise, stand, or walk. When lying down, she makes fairly normal leg movements. When trying to rise from the chair, she rocks up and down several times to rise. When commencing to walk, she makes several efforts to move her feet. After these efforts, she appears somewhat puzzled, as if searching for lost motor engrams, or the right button to press to initiate walking. The effort to progress may result only in stepping on the same spot, as if trying to free the feet from thick, sticky mud, the dancing bear gait. If she does progress, her feet stick to the floor as if magnetized. Some observers have called the combination of short steps, wide base, and difficulty picking up the feet (magnet sign) a frontal gait, an apraxic gait, or an ignition failure gait (Nutt et al., 1993). Factor et al. (2002) stated that many Pts previously described with such terms may have primary progressive freezing gait, but its neuropathologic basis is unknown. Overall, just the presence of a clinically evident gait disorder in the elderly and the rate that it worsens correlate with the risk of death (Wilson et al., 2002).
Some Pts have a syndrome of gait disorder, dementia, and urinary incontinence. They take small steps of reduced velocity and variable stride length, but their feet characteristically turn out (Stolze et al., 2001), a feature unusual in other gait disorders. Formerly called normal pressure hydrocephalus, Bret et al. (2002) emphasized that it can also occur in children and prefer the name chronic hydrocephalus.
To fully appreciate the astasia-abasia (astasia = not standing; abasia = not walking) of the hysteric Pt, the neophyte physician will have to witness it (Lempert et al., 1991; Keane, 1989). Often the Pt tilts, gyrates, and undulates all over the place, unwittingly proving by not falling during the marvelous demonstration of agility that strength, balance, coordination, and sensation have to be intact. However, do not mistake some of the bizarre involuntary movement disorders, in particular the dromedary gait of dystonia, or some focal seizures for hysteria. Lempert et al. (1991) listed six features of psychogenic gait:
Excessive slowness or hesitation
Exaggerated sway on the Romberg test, improved by distraction
Postures that waste energy
Extremely cautious, restricted steps, like walking on ice
Sudden buckling of the knees without falling
To learn how other mental illnesses affect the gait, just watch any group of Pts in a psychiatric hospital as they walk along the hall to the cafeteria. Hardily a single Pt steps out with a perfectly normal gait. This Pt, hopelessly moving along, sighing, shoulders sagging, head down looking at the floor, obviously suffers from depression (Sloman, 1982). The Pt over there wringing her hands and wrinkling her brow has an agitated depression. That unkempt middle-aged man, walking with small irregular, wincing steps placed gingerly on a wide base has spindly arms and legs that contrast with a disproportionate, pregnancy-like fullness of the abdomen. His alcoholism has caused mild shoulder girdle weakness, ascites, a rostral vermis syndrome, and a painful sensory neuropathy with hyperesthetic soles. That young adult Pt with a mild parkinsonian gait is probably a schizophrenic taking large doses of neuroleptic medication. That young woman, gesticulating as if conversing as she walks along, is a schizophrenic, attending to her hallucinations. She is underdosed or her medication has not yet taken hold. That next grim-faced Pt, walking cautiously and peering around suspiciously, suffers from severe paranoid schizophrenia. That child, running helter skelter, bumping into people and objects, giggling inappropriately, has an attention deficit disorder with hyperactivity. The teenager who, of inner necessity, steps on every crack, pats every door, and suddenly halts his progression to whirl around and utter expletives suffers from the disabling compulsions of severe Tourette's syndrome. That aged Pt with silvery white hair, confusion of purpose and direction, and marche à petit pas has, as you now know, organic dementia, most likely from senility or Alzheimer's disease. The retarded and autistic children have their gait peculiarities, often characterized by behavioral stereotypies such as hand flapping (Vilensky, 1981). Thus does the gait often disclose the mental and the neurologic status of the Pt.
Gentle reader, if we have overdone the gait examination a little, forgive us. If not quite the whole neurologic examination, nothing else discloses so much so quickly.
BIBLIOGRAPHY · Gait Analysis
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