The patient was a 63-year-old female who presented with pain about the low back, hip and an inability to place her right heel on the ground. The patient was walking with a cane. Prior to attending care, the patient had seen her PCP, a neurologist and an orthopedic surgeon. She had been under some form of care or consultation regarding this issue for the seven months.
Past diagnostic studies included CT scan of the head, MRI of the thoracic and lumbar spine, and plain films of the right hip. Brain CT scan revealed mild age-related atrophy and atherosclerotic intracranial carotid-artery calcifications. MRI of the cervical spine revealed broad central C5-C6 soft spondylotic disk protrusion deforming the spinal cord, broad central C4-5 disc protrusion deforming the cord, and right foraminal C3-4 spondylosis disc protrusion. MRI of the thoracic spine revealed mild bulging at T8-T9 and T10-T11. CT myelogram of the lumbar spine revealed advanced facet arthrosis involving primarily L4-L5 and (to a lesser extent) L5-S1, small focal central disk bulge L5-S1, shallow biforaminal focal disc bulges at L5-1, moderately severe central canal stenosis at L4-5 and annular bulging throughout the lower thoracic and lumbar spine. Although a myriad of spinal degenerative changes were present, there was no specific injury to the brain or compression to the spinal cord that would lead to the upper motor neuron symptomatology.
We then referred the patient for radiographs of the hip, which revealed moderate degenerative changes. The patient had not been given any answers as to the nature of her gait. Indeed, little mention was made of her gait in records.
On observing the patient's gait, an equinovarus foot, consistent with upper motor neuron lesion was noted. As Mayer and Esquenazi explain, "Equinovarus, the most common pathological posture in the lower extremity, presents with the foot and ankle turned down and in. Toe curling or clawing may exist as well. The patient has difficulty getting weight on to the heel, therefore disrupting normal gait. Dorsiflexion is limited in early and mid stance and prevents forward progression of the tibia over the stationary foot, resulting in hyperextension thrust of the knee, and dysrythmic and restrained forward progression of body mass. Lift-off rather than push-off occurs in terminal stance and a short contralateral step results. Knee flexion during pre-swing is deviant and early-swing foot drag may occur."1 Muscles that contribute to equinovarus include tibialis anterior, tibialis posterior, the long toe flexors, medial and lateral gastrocnemius, soleus, extensor hallux longus and peroneus longus.
In this patient, abduction of the hip was noted, as well as her tendency to swing the hip to complete the gait cycle. Persistent contraction was noted on EMG of the shin and calf musculature bilaterally. Although signs of upper motor-neuron lesion were noted [flexor and extensor spasm, co-contraction of agonist and antagonist groups and increased muscle stiffness leading to contracture (muscle over activity in the upper motor neuron syndrome], inconsistencies were noted, such as diminished reflexes.2
Following a brief course of treatment in which occasional brief but unsustained changes in the patient's gait were evident (i.e., periodic moments when the patient could plant her right heel), we had the patient consult with another neurologist. Following review of the above-mentioned MRI examinations, performance of a second EMG and discussion with the patient of stressors (her lack of employment and her husband's illness) consideration of conversion disorder was discussed. After a brief course of diazepam (Valium), the patient's gait had changed rapidly and has been sustained.
In conversion disorder, the patient's emotions become transformed into physical or sensory manifestations. Common presentations include blindness, deafness, paresis, sensory disturbances, ataxia, seizures and unconsciousness.3 This is not to be construed as malingering or consciously faking, but rather the mind converting emotions (usually anxiety) into a somatic problem.
This is not to say that all patients who present with an unusual array of symptoms have conversion disorder. However, it would be wise to look at the entire picture and discuss the congruence of symptoms with physical findings and patient stressors, and to be cognizant of the common manifestations of possible conversion disorder and keep an open dialogue with providers in other disciplines.
References
- Mayer N, Esquenazi A, Eds. "Muscle Overactivity in the Upper Motor Neuron Syndrome. http://ntiasiapacific.org/chapter_umns_print.htm.
- Ibid.
- Sweere JJ, Ed. Chiropractic Family Practice-A Clinical Manual. Gaithersburg Md.: Aspen Publishers, 1992.
