A 60-year-old male, who presents to the Physical Medicine and Rehabilitation (PM&R) clinic for difficulty with walking. He endorses two near fall episodes in the past 6 months, as well as difficulty when starting to walk and with turns.
Past medical/surgical history: Atrial fibrillation on anticoagulant (Afib on AC), diabetes, hypertension, lumbar stenosis s/p laminectomy, R Carpal tunnel release.
Allergies: Tylenol, Macrobid, contrast dye.
Medication: coumadin, metformin, Lopressor, Tamsulosin.
Family History: Noncontributory.
Social History: Patient lives at home with wife in a three-floor family house, with six steps to enter and 13 steps to third floor. The patient uses a rolling walker, as well as a cane for stairs and requires some assistance from his wife for the activity of daily living
Former smoker denies any alcohol (EtOH) or rec drug use.
BP: 130/75 mmHg, sitting, standing 120/70 mmHg, RR: 14/min, PR: 70 per min, Temp; 97° F, Ht: 5’5” Wt: 130 lbs, BMI 21 kg/m 2 .
Head, ear, eyes, nose, and throat (HEENT): Extraocular movement (EOM) full, no ptosis.
General: Alert, oriented and in no acute distress. Extremely fatigued.
Extremities: No edema, no skin rashes, no fasciculation seen.
Visual inspection: Muscular bulk appropriate for age with no focal weakness. No gross evidence of joint or tissue swelling.
Range of motion (ROM): Full passive range of motion in all major joints of bilateral upper extremities (BUEs). ROM of the neck: Complete in all directions.
Mental status: AO×3, hypokinetic dysarthria, hypophonia, speech fluent, comprehension intact, masked faces.
Cranial nerves: EOM intact, pupils equal and reactive to light and accommodation, reduced facial expression, tongue midline.
Motor: 5/5 strength in b/l upper/lower extremities; cogwheeling bilaterally R>L in upper extremity.
Reflexes: 1+ in b/l upper and lower extremities.
Plantar reflex: Symmetrical, plantar downgoing.
Sensory: Intact to light touch to b/l upper/lower extremities.
Coordination: Negative Romberg, able to do finger to nose.
Pill rolling resting tremor, tone was normal.
Gait: A decrease in step length and height stooped posture and reduced arm swing. Short and shuffling gait with a tendency to fall backward, positive retropulsion test. Episodes of freezing and difficulty completing turns.
The initial focus in the general approach to a patient with gait dysfunction should be on history (falls in the past, activity limitation, time frame symptoms noted), past medical history, and physical examination. The physical examination should include a full neurologic exam, comprehensive musculoskeletal exam, and cardiovascular including peripheral arterial disease (claudication), and orthostatic hypotension. Medications should also be reviewed closely. It is important to differentiate between neurologic and musculoskeletal disorders, as well as from medical conditions affecting the neuromusculoskeletal system. Always keep in mind that gait disorders, especially in geriatric population, may have several causes.
Watching the patient walk is important to examine the gait cycle. Monitor the number of steps in a period of time (cadence), comfortable walking speed, stride length (the distance between any two successive points of heel contact of the same foot) and stride width (the side-to-side distance between the line of a step of the two feet), and stride angle.
Specific gait patterns associated with particular diseases can provide us with vital clues towards diagnosis ( Table 12.1 ).
|Antalgic/arthritic gait||To avoid pain, weight is put on the affected leg for as short a time as possible, resulting in a limp|
|Cerebellar ataxic gait||Broad based stance and gait, variable step length, insecure and wobbly|
|Sensory ataxia||Broad based, while walking in a dark or performing the Romberg test and eliminating the visual input, can lead to worsening imbalance|
|Cervical spondylotic myelopathy||Decreased speed walk, with shorter stride lengths and longer double support duration|
|Psychogenic gait disorders||Mimic a very insecure gait, temporary improvement or complete resolution of symptoms can be seen while the patient is distracted or thinks he or she is unobserved|
|Vestibulopathic gait||The legs are slightly spread, and stride length is slightly reduced, Unterberger test positive, deviation to the affected side|
|Apraxic/dysexecutive gait||Difficulty and hesitation in initiating the gait, short shuffling gait, and freezing|
|Choreatic gait disorder||Sudden involuntary movements in knee and hip flexors leads to dancelike swaying movements|
|Parkinsonian gait||Decrease in step length and height, stooped posture, and reduced arm swing, en bloc turn|
|Neuromuscular gait||Instability of the weight-bearing hip and causes the nonweight-bearing side to drop (Trendelenburg sign), excessive side to side trunk motion and a waddling gait|
|Spastic gait/unilateral||Extensor synergy pattern with knees extended, ankles plantar flexed and inverted, the ipsilateral arm is often flexed (circumduction)|
|Spastic gait/bilateral||Thighs adducted because of increased tone with scissoring across the midline|
Common Differential Diagnoses
Antalgic gait/arthritic gait —a limp that develops in response to pain. This can be caused by osteoarthritis in the lower extremity, ankle sprains, foot stress fracture, and so on. Because of pain on weight bearing, to avoid pain; weight is quickly shifted from the affected leg to the other leg. ,
Cerebellar ataxic gait —presents as an insecure wobbly, broad-based stance and gait. Stooped posture accompanied by a cautious walk with variable step length is noted. Midline lesions in the cerebellar vermis can lead to truncal ataxia. Clinical findings include difficulty with finger to nose test, finding of positive Romberg test, and nystagmus.
Proprioception loss —can lead to sensory ataxia. It can be seen in dorsal column lesions and sensory neuropathy. Without visual input, such as walking into a dark room, a significant worsening of imbalance can be seen. Therefore providing visual input or feedback mechanisms like foot slamming against the ground can be used as a compensatory strategy.
Cervical spondylotic myelopathy —the most common form of spinal cord dysfunction in people over 55 years of age. Usually patient presents with weakness in the lower extremities, accompanied by upper motor neuron signs (corticospinal and spinocerebellar tract dysfunction) and spasticity.
Functional neurologic disorder/psychogenic gait disorder —can present with unusual and inconsistent neurologic findings along with insecure gait. The diagnosis of exclusion should be the approach to these patients. One important confirmatory finding is a total improvement of neurologic signs while being distracted. ,
Unilateral/bilateral vestibular dysfunction —leads to vestibulopathic gait. Positive Unterberger’s stepping test (asking the patient to step in place for 20–30 seconds) and because of lack of vestibular ocular reflex, one feels like walking in darkness with a propensity to fall. ,
Higher-level gait disorder/apraxic gait disorder —basically a failure of motor programming because of frontal lobe dysfunction. Hesitation and difficulty in initiating the gait, short shuffling gait, and freezing are the characteristic features. ,
Choreatic gait disorder —a manifestation of Huntington disease and tardive dyskinesia and levodopa-induced dyskinesia. Sudden involuntary movements in the knee and hip flexors lead to dancing like wormy movements.
Parkinson gait —characterized by shuffling gait, decrease in step length and height. Reduced arm swing and stooped posture have been attributed to the imbalance. Significant difficulty while initiating steps, reaching obstacles and turns (en bloc turn) happens and can lead to falling. Multiple system atrophy (MSA) is a combination of parkinsonism and cerebellar signs with orthostatic hypotension. ,
Neuromuscular gait disorder —happens in cases of myopathy and proximal muscle weakness. Weakness in pelvic stabilizer muscles leads to a drop of weight-bearing side (Trendelenburg sign) and side-to-side trunk motion (waddling gait). Knee hyperextension gait can be seen in quadriceps muscle weakness. Ankle dorsiflexors weakness leads to high steppage gait with excessive foot lifting off the floor during the swing phase.
Unilateral/bilateral lesions —lesions in the corticospinal tract at any level can lead to spastic gaits. In cases of unilateral cerebral cortex lesion, circumduction is manifested as extended knees and flexed inverted ankle plantar flexors. In bilateral lesions, adducted thighs and scissoring gait can lead to spastic paraparesis.
Our patient states that he has been struggling with his walking, including difficulty initiating walking, difficulty with obstacles, and in turning with reports of near fall episodes in the past 6 months. Blood pressure medication or tamsulosin can cause orthostatic changes, which can lead to falls. Given he is on anticoagulation, he is at higher risk for subdural hematomas after a fall and fall prevention is crucial. His past history of diabetes mellitus (DM), atrial fibrillation (which increases risk of stroke), and spinal stenosis may lead to the consideration of a neuropathic or brain disorder, or a spinal cord disorder, but his examination suggests other causes. On his examination, he is noted to have full strength, normal deep tendon reflexes, and no distal sensory abnormalities. Neuropathy is less likely with normal sensory, motor, and deep tendon reflexes, and without upper motor signs, cord compression is unlikely. The patient examination notes include tremor, cog wheeling, and a shuffling gait, which is typical for parkinsonism.
The most common cause of parkinsonism symptoms is Parkinson disease (PD) and this can lead to progressive disability. It affects males 1.5 times more than females. PD is a clinical diagnosis, without a specific imaging study or laboratory test to confirm the diagnosis at this time. Clinical features include pill-rolling, resting tremor, unilateral involvement which over time can develop to asymmetric bilateral symptoms, olfactory dysfunction, and beneficial positive response to levodopa support the diagnosis of PD. ,
Atypical parkinsonian syndromes, especially early in the course, can be misdiagnosed as PD. These disorders include MSA, progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), and dementia with Lewy bodies (DLB) , ( Table 12.2 ).
|Atypical Parkinsonian Types||Features|
|Multiple system atrophy (parkinsonian type)|
|Progressive supranuclear palsy|
|Corticobasal ganglionic degeneration|
|Lewy body disease (parkinsonian dementia)|