The gag reflex—a protective mechanism that prevents aspiration of food, fluid, and vomitus— normally can be elicited by touching the posterior wall of the oropharynx with a tongue depressor or by suctioning the throat. Prompt elevation of the palate, constriction of the pharyngeal musculature, and a sensation of gagging indicate a normal gag reflex. An abnormal gag reflex—either decreased or absent—interferes with the ability to swallow and, more important, increases susceptibility to life-threatening aspiration.

An impaired gag reflex can result from any lesion that affects its mediators—cranial nerves IX (glossopharyngeal) and X (vagus), the pons, or the medulla. It can also occur during a coma, in muscle diseases such as severe myasthenia gravis, or as a temporary result of anesthesia or drug or alcohol use.

If you detect an abnormal gag reflex, immediately stop the patient’s oral intake to prevent aspiration. Quickly evaluate his level of consciousness (LOC). If it’s decreased, place him in a side-lying position to prevent aspiration; if not, place him in Fowler’s position. Have suction equipment ready to use.

A bizarre gait has no obvious organic cause; rather, it’s produced unconsciously by a person with a somatoform disorder (such as hysterical neurosis) or consciously by a malingerer. The gait has no consistent pattern. It may mimic an organic impairment but characteristically has a more theatrical or bizarre quality with key elements missing, such as a spastic gait without hip circumduction, or leg “paralysis” with normal reflexes and motor strength. Its manifestations may include wild gyrations, exaggerated stepping, leg dragging, or mimicking unusual walks, such as that of a tightrope walker.

Propulsive gait is characterized by a stooped, rigid posture—the patient’s head and neck are bent forward; his flexed, stiffened arms are held away from the body; his fingers are extended; and his knees and hips are stiffly bent. During ambulation, this posture results in a forward shifting of the body’s center of gravity and consequent impairment of balance, causing increasingly rapid, short, shuffling steps with involuntary acceleration (festination) and lack of control over forward motion (propulsion) or backward motion (retropulsion).

Propulsive gait is a cardinal sign of advanced Parkinson’s disease; it results from progressive degeneration of the ganglia, which are primarily responsible for smooth muscle movement. Because this sign develops gradually and its accompanying effects are often wrongly attributed to aging, propulsive gait commonly goes unnoticed or unreported until severe disability results.

Ask the patient (or a family member if the patient can’t answer) about the onset and duration of the gait. Has it progressively worsened or remained constant? Ask about a history of trauma, including birth trauma, and neurologic disorders. Thoroughly evaluate motor and sensory function and deep tendon reflexes (DTRs) in the legs.

♦ Cerebral palsy. In the spastic form of this disorder, patients walk on their toes with a scissors gait. Other features include hyperactive DTRs, increased stretch reflexes, rapid alternating muscle contraction and relaxation, muscle weakness, underdevelopment of affected limbs, and a tendency toward contractures.

♦ Cervical spondylosis with myelopathy. Scissors gait develops in the late stages of this degenerative disease and steadily worsens. Related findings mimic those of a herniated disk: severe low back pain, which may radiate to the buttocks, legs, and feet; muscle spasms; sensorimotor loss; and muscle weakness and atrophy.

♦ Hepatic failure. Scissors gait may appear several months before the onset of hepatic failure. Other findings may include asterixis, generalized seizures, jaundice, purpura, dementia, and fetor hepaticus.

♦ Multiple sclerosis. Progressive scissors gait usually develops gradually, with periodic remissions. Characteristic muscle weakness, usually in the legs, ranges from minor fatigability to paraparesis with urinary urgency and constipation. Related findings include facial pain, visual disturbances, paresthesia, incoordination, and loss of proprioception and vibration sensation in the ankle and toes.

♦ Pernicious anemia. Scissors gait sometimes occurs as a late sign in untreated pernicious anemia. Besides this disorder’s classic triad of symptoms—weakness, sore tongue, and numbness and tingling in the extremities—the patient may exhibit pale lips, gums, and tongue; faintly jaundiced sclerae and pale to bright yellow skin; impaired proprioception; incoordination; and vision disturbances (diplopia, blurring).

♦ Spinal cord trauma. Scissors gait may develop during recovery from partial spinal cord compression, particularly with an injury below C6. Associated findings may include sensory loss or paresthesia, muscle weakness or paralysis distal to the injury, and bladder and bowel dysfunction.

♦ Spinal cord tumor. Scissors gait can develop gradually from a thoracic or lumbar tumor. Other findings reflect the location of the tumor and may include radicular, subscapular, shoulder, groin, leg, or flank pain; muscle spasms or fasciculations; muscle atrophy; sensory deficits, such as paresthesia and a girdle sensation of the abdomen and chest; hyperactive DTRs; bilateral Babinski’s reflex; spastic neurogenic bladder; and sexual dysfunction.

♦ Stroke. Scissors gait occasionally develops during the late recovery stage of bilateral occlusion of the anterior cerebral artery. The patient may also display leg muscle paraparesis and atrophy, incoordination, numbness, urinary incontinence, confusion, and personality changes.

♦ Syphilitic meningomyelitis. Scissors gait appears late in this disorder and may improve with treatment. The patient may also experience sensory ataxia, changes in proprioception and vibration sensation, optic atrophy, and dementia.

♦ Syringomyelia. Scissors gait usually occurs late in this disorder along with analgesia and thermanesthesia, muscle atrophy and weakness, and Charcot’s joints. Other effects may include loss of fingernails, fingers, or toes; Dupuytren’s contracture of the palms; scoliosis; and clubfoot. Skin in the affected areas is typically dry, scaly, and grooved.

Because of the sensory loss associated with scissors gait, provide meticulous skin care to prevent skin breakdown and pressure ulcer formation. Also, give the patient and his family complete skin care instructions. If appropriate, provide bladder and bowel retraining.

Promote daily active and passive range-ofmotion exercises. Refer the patient to a physical therapist, if appropriate, for gait retraining and for possible application of in-shoe splints or leg braces to maintain proper foot alignment for standing and walking.

The major causes of scissors gait in children are cerebral palsy, hereditary spastic paraplegia, and spinal injury at birth. If spastic paraplegia is present at birth, scissors gait becomes apparent when the child begins to walk, which is usually later than normal.

Spastic gait—sometimes referred to as paretic or weak gait—is a stiff, foot-dragging walk caused by unilateral leg muscle hypertonicity. This gait indicates focal damage to the corticospinal tract. The affected leg becomes rigid, with a marked decrease in flexion at the hip and knee and possibly plantar flexion and equinovarus deformity of the foot. Because the patient’s leg doesn’t swing normally at the hip or knee, his foot tends to drag or shuffle, causing his toes to scrape on the ground. To compensate, the pelvis on the affected side tilts upward in an attempt to lift the toes, causing the patient’s leg to abduct and circumduct. Also, arm swing is hindered on the same side as the affected leg.

Spastic gait usually develops after a period of flaccidity (hypotonicity) in the affected leg. Whatever the cause, spastic gait is usually permanent.

Steppage gait typically results from footdrop caused by weakness or paralysis of pretibial and peroneal muscles, usually from lower motor neuron lesions. Footdrop causes the foot to hang with the toes pointing down, causing the toes to scrape the ground during ambulation. To compensate, the hip rotates outward and the hip and knee flex in an exaggerated fashion to lift the advancing leg off the ground. The foot is thrown forward and the toes hit the ground first, producing an audible slap. Steppage gait usually has a regular rhythm, with even steps and normal upper body posture and arm swing. It can be unilateral or bilateral and permanent or transient, depending on the site and type of neural damage.

Ask the patient (or a family member if the patient is a young child) when the gait first appeared and if it has recently worsened. To determine the extent of pelvic girdle and leg muscle weakness, ask if the patient falls frequently or has difficulty climbing stairs, rising from a chair, or walking. Also, find out if he was late in learning to walk or holding his head upright. Obtain a family history, focusing on problems of muscle weakness and gait and on congenital motor disorders.

Inspect and palpate leg muscles, especially in the calves, for size and tone. Check for a
positive Gowers’ sign (an inability to lift the trunk without using the hands and arms to brace and push), which indicates pelvic muscle weakness. Next, assess motor strength and function in the shoulders, arms, and hands, looking for weakness or asymmetrical movements.

♦ Congenital hip dysplasia. Bilateral hip dislocation produces a waddling gait with lordosis and pain.

♦ Muscular dystrophy. In Duchenne’s muscular dystrophy, waddling gait becomes clinically evident by ages 3 to 5. The gait worsens as the disease progresses, until the child loses the ability to walk and needs a wheelchair, usually between ages 10 and 12. Early signs are usually subtle: delay in learning to walk, frequent falls, gait or posture abnormalities, and intermittent calf pain. Common later findings include lordosis with abdominal protrusion, a positive Gowers’ sign, and equinovarus foot position. As the disease progresses, its effects become more prominent; they commonly include rapid muscle wasting beginning in the legs and spreading to the arms (although calf and upper arm muscles may become hypertrophied, firm, and rubbery), muscle contractures, limited dorsiflexion of the feet and extension of the knees and elbows, obesity and, possibly, mild mental retardation. If kyphoscoliosis develops, it may lead to respiratory dysfunction and, eventually, death from cardiac or respiratory failure.

In Becker’s muscular dystrophy, waddling gait typically becomes apparent in late adolescence, slowly worsens during the third decade, and culminates in total loss of ambulation. Muscle weakness first appears in the pelvic and upper arm muscles. Progressive wasting with selected muscle hypertrophy produces lordosis with abdominal protrusion, poor balance, a positive Gowers’ sign and, possibly, mental retardation.

In facioscapulohumeral muscular dystrophy, which usually occurs late in childhood or during adolescence, waddling gait appears after muscle wasting has spread downward from the face and shoulder girdle to the pelvic girdle and legs. Earlier effects include progressive weakness and atrophy of facial, shoulder, and arm muscles; slight lordosis; and pelvic instability.

♦ Spinal muscle atrophy. In Kugelberg-Welander syndrome, waddling gait occurs early (usually after age 2) and typically progresses slowly, culminating in total loss of ambulation up to 20 years later. Related findings may include muscle atrophy in the legs and pelvis, progressing to the shoulders; a positive Gowers’ sign; ophthalmoplegia; and tongue fasciculations.

In Werdnig-Hoffmann disease, waddling gait typically begins when the child learns to walk. Reflexes may be absent. The gait progressively worsens, culminating in complete loss of ambulation by adolescence. Associated findings include lordosis with abdominal protrusion and muscle weakness in the hips and thighs.

Although there’s no cure for waddling gait, daily passive and active muscle-stretching exercises should be performed for both arms and legs. If possible, have the patient walk at least 3 hours each day (with leg braces if necessary) to maintain muscle strength, reduce contractures, and delay further gait deterioration. Stay near the patient during the walk, especially if he’s on unfamiliar or uneven ground. Provide a balanced diet to maintain energy levels and prevent obesity. Because of the grim prognosis associated with muscular dystrophy and spinal muscle atrophy, provide emotional support for the patient and his family.