W | Anesthesia Key

Walking Difficulties

When a patient complains of difficulty walking, visualize the anatomic components of the leg: skin, muscle, arteries, veins, bones, joints, and peripheral nerves. Going one step further, follow the peripheral artery to its origin (femoral artery, aorta, and so forth) and the peripheral nerve to its origin in the spinal cord, and then follow its secondary connections to the cerebellum and cerebrum. Now it is possible to recall the causes of difficulty walking as the patient is being examined.

Skin: Look for calluses, infectious ulcers, and deformities of the feet.
Muscle: Check for possible myositis, contusions, and muscular atrophy or dystrophy. The gait of muscular dystrophy is slapping and waddling, and there is a pelvic tilt forward.
Arteries: Peripheral arteriosclerosis and Buerger disease will often be detected by palpation of the dorsalis pedis and tibialis pulses. However, do not forget to feel the femoral arteries (to rule out Leriche syndrome) and popliteal arteries. Listening to the heart may determine a cause for a peripheral embolism.
Veins: Dilated varicose veins will be obvious, but checking for a positive Homan sign will be necessary to rule out deep vein phlebitis.
Bones: Osteomyelitis and sarcomas or metastatic disease of the bone will usually present with significant pain and make the patient extremely reluctant to walk. A mass or deformity in the bone is usually palpable.
Joints: Osteoarthritis, gout, and rheumatoid arthritis of the knee are not hard to detect. The gait in diseases in any joint in the leg is a limp. The cause of pain in the other joints may be more difficult to appraise even with an x-ray film. Nevertheless, these and a full joint disease workup will help (see page 274). An osteoarthritic spur of the heel may be found. Bursitis in numerous areas should be looked for. Congenital lesions such as slipped epiphysis, dislocation of the hip, and aseptic necrosis should be considered in children.
Peripheral nerves: A peripheral neuropathy from alcohol or diabetes will cause a steppage gait (due to moderate or severe foot drop), and traumatic or lead neuropathy may cause an overt foot drop. The atrophy of the muscles without fasciculations will help in the diagnosis of these as well as of Dejerine–Sottas hereditary neuropathy and Charcot–Marie–Tooth disease. Sensory changes (glove and stocking anesthesia and analgesia) are also useful.
Spinal cord: These diseases present with different types of gaits. There may be a wide-based ataxic gait with a positive Romberg sign in dorsal column and dorsal root involvement, suggesting tabes dorsalis and pernicious anemia. There may be a wide-based reeling ataxia with a negative Romberg sign, suggesting cerebellar disease such as Friedreich ataxia. A spastic gait suggests amyotrophic lateral sclerosis, multiple sclerosis, and diseases with diffuse spinal cord involvement such as anterior spinal artery occlusion. A spastic ataxic gait is typical of multiple sclerosis. Other causes of a spastic gait are compression by tumors, cervical spondylosis, or disks; transverse myelitis; traumatic conditions such as fractures; hematomas; and epidural abscesses. The gait of herniated disks of the lumbosacral spine is usually a list to the left or right or a limp. Loss of the ankle or knee jerk, dermatomal sensory loss, and erector spinae muscle spasm will help in this diagnosis. If there is a cauda equina tumor or poliomyelitis, bladder symptoms are usually present as well. Other conditions of the lumbosacral spine disturb the gait (limp) and include osteoarthritis, rheumatoid spondylitis, spondylolisthesis, metastatic tumors, tuberculosis, and multiple myeloma.
Secondary connections to the brain: Involvement of the pyramidal tracts in the brain often produces a hemiplegic gait where the weak or spastic leg is dragged along the floor. The gait of vestibular disease is ataxic and reeling during an attack. Cerebellar disease has already been discussed. Tumors or abscesses here and alcoholic and phenytoin sodium toxicity may cause a cerebellar ataxia. Multiple sclerosis is another condition that may result in this type of a gait. Bilateral cerebral involvement in cerebral arteriosclerosis or presenile and senile dementia produces the short-stepped gait of Marche à petit pas. Cerebral palsy may cause a scissor gait. The spastic, shuffling gait of Parkinsonism with propulsion and retropulsion is not easily missed.

Approach to the Diagnosis

The clinical picture can help to pinpoint the diagnosis in many cases. If the difficulty develops after walking a block or a certain distance, the patient may have neurogenic or vascular claudication, and spinal stenosis or peripheral arteriosclerosis is suspected. If there is swelling and crepitus of the knee joints, an arthritic condition is likely. Muscular atrophy and fasciculations suggest progressive muscular atrophy, whereas atrophy with sensory changes suggests peripheral neuropathy. A spastic ataxic gait with blurred vision or scotomata suggests multiple sclerosis.

The initial workup of a patient with walking difficulties will depend on the clinical picture. If there is possible peripheral vascular disease, Doppler studies and possible
femoral angiography or aortography need to be done. If a patient is suspected of having a deep vein thrombosis, he or she should be hospitalized and Doppler studies, impedance plethysmography, or contrast venography will be done. If the patient has clinical radiculopathy, a computed tomography (CT) scan or magnetic resonance imaging (MRI) of the lumbar spine will be done to rule out a herniated disk. If multiple sclerosis is suspected, an MRI of the brain or spinal cord will be done depending on the level of the involvement clinically.

Walking difficulties.

Other Useful Tests

Complete blood count (CBC) (pernicious anemia)
Drug screen (drug abuse)
Sedimentation rate (inflammation)
Blood lead level (lead neuropathy)
Glucose tolerance test (diabetic neuropathy)
Antinuclear antibody (ANA) analysis (collagen disease)
Chemistry panel (cirrhosis of the liver, muscle disease)
Schilling test (pernicious anemia)
Electromyogram (EMG) (muscle dystrophy, peripheral neuropathy)
Spinal tap (tumor, multiple sclerosis, neurosyphilis)
Urine porphobilinogen (porphyria)
X-ray of joints (arthritis)
Bone scan (osteomyelitis, neoplasm)
Neurology consult
Orthopedic consult

Walking difficulties.

Weakness and Fatigue, Generalized

The analysis of the causes of weakness depends on a knowledge of both anatomy and biochemistry. Strength depends on an intact healthy muscle, peripheral nerve, and lower
and upper motor neuron pathways and a functioning myoneural junction. Thus, general weakness may develop in muscle disease (analyzed according to etiologic categories in Table 60), myoneural junction disease (myasthenia gravis and Eaton–Lambert syndrome), peripheral neuropathies (Table 60), anterior horn disease (poliomyelitis, lead poisoning, and spinal muscular atrophy), and diffuse disease of the pyramidal tracts, such as multiple sclerosis. Parkinson disease fatigues the muscles by the tremor and spasticity it induces.

However, this is only half the story. A muscle cannot be strong unless there is adequate intake and absorption of glucose or proper tissue use of glucose (insulin action). Malnutrition and malabsorption syndrome are excellent examples of the former, whereas diabetes mellitus, acromegaly, Cushing disease, and insulinomas are good examples of the latter. The muscle must also have an adequate supply of oxygen. Thus chronic lung disease (see page 112) of any cause, congestive heart failure (CHF) of any cause, and chronic anemia may all produce weakness because of decreased supply of oxygen to the muscles. It is also vital to have the proper minerals surrounding the muscle fiber. Most important are proper sodium, potassium, and calcium balance. Thus, any condition causing a low-sodium syndrome (CHF or diuretics), a high-or low-potassium syndrome (Addison disease, diuretics, aldosterone tumors), or a high or low calcium balance (hyperparathyroidism, metastatic carcinoma of the bone, and hypoparathyroidism) may produce weakness. It is well known that vitamin B deficiency causes fatigue and neuropathy. Recent research indicates that vitamin D deficiency is also a cause of fatigue.

Weakness develops in liver disease because of intermittent hypoglycemia or inability to dispose of toxins. In uremia, the problem is not only poor ability to get rid of toxins, but the altered electrolyte media of sodium, potassium, calcium, and magnesium. In hypermetabolic states, there may be a breakdown of muscle to release protein for nutrition when intake is not adequate to meet demands of vital organs. Thus, in hyperthyroidism, chronic inflammatory and febrile diseases, and diffuse neoplastic disease, weakness is a common manifestation.

No discussion of weakness would be complete without mentioning the psychogenic causes of weakness such as depression and chronic anxiety states. Finally, smoking and chronic ingestion of caffeine, toxins, and various proprietary drugs (e.g., aspirin) are, of course, related to psychogenic disturbances and should always be considered in the differential diagnosis.

Approach to the Diagnosis

The association of other symptoms and signs with generalized weakness and fatigue is very important in pinning down a diagnosis. Generalized lymphadenopathy and fatigue suggest infectious mononucleosis, lymphoma, or tuberculosis or other chronic infection such as acquired immunodeficiency syndrome (AIDS). Weakness, weight loss, and polyphagia with polyuria and polydipsia would suggest hyperthyroidism or diabetes mellitus. Generalized weakness with polyuria and no significant weight loss suggests hyperparathyroidism. Weakness with pallor suggests some type of anemia. Weakness and weight loss without polyuria or polyphagia suggest malignancy or malabsorption syndrome. Weakness with other significant neurologic signs and symptoms prompts the consideration of muscular dystrophy, amyotrophic lateral sclerosis, or multiple sclerosis. Weakness with drug or alcohol use prompts the investigation of drug or alcohol abuse. Caffeine, especially in large quantities, can also cause significant weakness and chronic fatigue.

The initial workup of weakness and fatigue requires a CBC, sedimentation rate, drug screen, chemistry panel, thyroid profile, serum and urine osmolality, ANA, chest x-ray, and echocardiogram. If muscular dystrophy or dermatomyositis is suspected, urine tests for creatinine, creatine, and myoglobin can be done. The Lambert–Eaton syndrome can be diagnosed by a VCGG radioimmunoassay. Ultimately, a muscle biopsy may be indicated. If myasthenia gravis is suspected, serum for acetylcholine receptor antibody may be done. If Addison disease is suspected, a serum cortisol test before and after ACTH stimulation may be done. A 24-hour urine aldosterone level may be done to exclude primary aldosteronism. Serum parathyroid hormone (PTH) may be done to exclude hyperparathyroidism.

It would be wise to consult an infectious disease specialist before ordering an expensive workup. It would also be wise to consult an oncologist when searching for a malignancy before ordering an expensive workup.

When all tests have negative findings, many clinicians have been tempted to make a diagnosis of chronic fatigue syndrome. It is questionable whether this is truly a disease or not.

Other Useful Tests