G | Anesthesia Key

Gait Disturbances

The anatomic location of the lesion in a gait disturbance depends on the type of disturbance.

Spastic gait: In this type of lesion, both feet shuffle along the floor in short steps and the legs are close together moving in a scissors-like fashion. Spastic gait is caused by lesions of both pyramidal tracts anywhere from the lower spinal cord to the brain stem and brain. The principal disorders are the following:
- In the cord: Multiple sclerosis, amyotrophic lateral sclerosis, spinal cord tumors, syringomyelia, and cervical trauma or spondylosis
- In the brainstem: Tumors, basilar artery thrombosis, multiple sclerosis, platybasia, and progressive lenticular degeneration
- In the brain: Cerebral arteriosclerosis, cerebral palsy, general paresis, and senile or presenile dementia
Hemiplegic gait: One foot is dragged above the floor, swinging out in a semicircular fashion. This is due to involvement of only one pyramidal tract, usually in the brain. Cerebral hemorrhage, thrombosis, emboli, and space-occupying lesions may be the culprits. Multiple sclerosis, early cervical cord tumor, or disc may do the same.
Steppage gait: Because of the weakness of dorsiflexion of both feet, the patient has to lift the foot high to avoid tripping. The lesion is a diffuse peripheral neuropathy that may be caused by lead intoxication, alcoholism, diabetes, porphyria, perineal muscular atrophy, or a cauda equina tumor. There are many other causes of peripheral neuropathy discussed on page 334.
Limping gait: Pain in one lower extremity due to bone disease, sciatica, hip disease, knee joint disease, or ankle and foot disorders of all types may cause favoring of the painful limb and quickening of the stride on that side so the victim can get back on the healthy limb. Osteoarthritis of the hip or knee, a herniated disc, an osteoarthritic spur of the heel, a sprained ankle, and fracture of any of the bones of the limb are typical conditions causing this type of gait. In children, consider child abuse.
Ataxic gait: The gait is wide-based, clumsy, and staggering. An ataxic gait may be sensory or cerebellar. Sensory ataxia is due to a lesion of the dorsal columns, such as tabes dorsalis, pernicious anemia, or a spinal cord tumor. In sensory ataxia, the patient walks carefully with his eyes fixed on the ground. Cerebellar ataxia is due to involvement of the spinocerebellar tracts and cerebellum. This occurs in hereditary cerebellar ataxia, Friedreich ataxia, cerebellar tumors, multiple sclerosis, and alcoholic cerebellar atrophy. In a cerebellar ataxia, the patient reels about when walking, and it is not much more difficult to walk with the eyes closed. Multiple sclerosis and syringomyelia may involve the dorsal columns, pyramidal and spinocerebellar tracts, or cerebellum, producing a mixed spastic–ataxic gait.
Muscular dystrophy gait: This is wide-based with a pelvic tilt forward as if the patient is trying to “show off,” but the feet are lifted from the ground with difficulty and there is waddling or rolling from side to side.
Extrapyramidal disease gait: The gait is short-stepped and spastic, and the feet shuffle along the ground. The patient may tilt forward with the trunk and head bent toward the ground, causing acceleration (propulsion); at times, the reverse may occur (retropulsion). In Huntington chorea, the gait is clownish and grotesque, as if the patient were drunk but playing games.

Approach to the Diagnosis

The workup depends on the presence or absence of other neurologic signs. If a peripheral nerve lesion is suspected, a workup for diabetes and a careful history for alcoholism and porphyria are expected. A suspected spinal cord lesion requires x-rays of the spinal column, spinal tap, Schilling test, and possibly a myelogram or magnetic resonance imaging (MRI). When the lesion is believed to be in the brain or brain stem, an MRI or computed tomography (CT) scan is almost axiomatic before a spinal tap or other radiocontrast studies are considered. A neurologist or neurosurgeon can best decide how the workup should be conducted.

Other Useful Tests

Complete blood count (CBC) (pernicious anemia)
Sedimentation rate (epidural abscess, collagen disease)
Fluorescent treponemal antibody absorption (FTA-ABS) test (neurosyphilis)
Tuberculin test (tuberculosis of the spinal column)
Chemistry panel (muscle disease, cirrhosis)
Serum protein electrophoresis (multiple myeloma)
Blood lead level (lead neuropathy)
Antinuclear antibody (ANA) analysis (collagen disease)
Rheumatoid arthritis (RA) test
Serum B₁₂ and folate levels (pernicious anemia)
Urine porphobilinogen (porphyria)
24-hour urine for creatinine and creatine (muscular dystrophy)
Muscle biopsy (muscular dystrophy, collagen disease)

Gait disturbances.

Case Presentation #34

A 42-year-old black man complained of difficulty walking and weakness of all four extremities which had become progressively worse over the last 3 years. He denied any pain, numbness, or tingling, but his vision had also deteriorated somewhat in the same period of time.

Question #1. Utilizing the methods discussed above, what is your differential diagnosis?

Neurologic examination revealed weakness, atrophy, and diminished reflexes of all extremities. There were bilateral cataracts and testicular atrophy.

Question #2. What is your diagnosis?

(See Appendix B for the answers.)

Gangrene

The mnemonic VINDICATE will help formulate a useful list of possible causes of gangrene.

V—Vascular: Gangrene is seen in peripheral arteriosclerosis, Buerger disease, thrombosis of the large arteries such as the femoral artery, thrombosis of the terminal aorta, and arterial embolism.
I—Infection: Gas gangrene is typically produced by Clostridium perfringens and other clostridia. Streptococci, peptostreptococci, and staphylococci can produce progressive bacteria-synergistic gangrene.
N—Neoplasm and neurological: Cryoglobulinemia and multiple myeloma are associated with the Raynaud phenomenon producing gangrene in the fingers. Peripheral neuropathy, syringomyelia, transverse myelitis, and tabes dorsalis may be associated with gangrene.
D—Degenerative diseases are not generally associated with gangrene.
I—Intoxication should bring to mind the gangrene associated with the use of ergot alkaloids.
C—Congenital disorders are not usually associated with gangrene.
A—Autoimmune disease: Lupus erythematosus, scleroderma, periarteritis nodosa, and RA may be associated with the Raynaud phenomenon and gangrene.
T—Trauma: Laceration of a major artery to an extremity or pressure from splints may cause gangrene. Extreme cold will produce gangrene from frostbite.
E—Endocrine disorders bring to mind the well-known diabetic gangrene.

Approach to the Diagnosis

All patients should have a CBC, sedimentation rate, venereal disease research laboratory (VDRL) test, chemistry panel, and serum protein electrophoresis. In cases of Raynaud phenomenon, an ANA and RA titer should also be done. Allen test is also helpful. Aerobic and anaerobic cultures of exudates from the wound should also be taken. Plain x-rays of the area involved are recommended. If an embolism or obstruction of the large arteries is suspected, contrast angiography needs to be done. An ice water test, Sia water test, and serum immunoelectrophoresis will be useful in cases of the Raynaud phenomenon. A rheumatology consult is wise.

Gigantism

The differential of this symptom can be developed physiologically by overactivity or underactivity of an endocrine gland. Thus, overactivity of the pituitary gland (as in eosinophilic adenomas of the pituitary) causes gigantism from too much growth hormone, whereas underactivity of the testicles (as in Klinefelter syndrome) produces a tall individual because the inadequate secretion of testosterone delays closure of the epiphysis. Tumors of the adrenal cortex, testicle, and pineal gland may produce macrogenitosomia or prepubertal gigantism by stimulation of overgrowth by androgens and estrogens only to lead to ultimate dwarfism by premature closure of the epiphysis. Primary gigantism is like the gigantism of plants and flowers; genetic arachnodactyly is also a genetic form of gigantism, although it is a true disease and is associated with dislocation of the lens.

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