Gait Disorders
INVESTIGATIONS—SPECIFIC MRI Brain/Spinal Cord
• The most common initial imaging test is a brain/spinal MRI scan. This test enables to Gait Disorders 139
Diagnosis: A Symptom-based Approach in Internal Medicine 140
look for structural abnormalities, stroke, or tumors
• Particularly useful to detect tumors of the posterior fossa, brainstem, and MS. Also helpful to exclude other causes of neurological deficit, e.g. arteriovenous malformation, including lesions causing compression of the spinal cord.
CT Brain
• Useful in acute stroke and to exclude mass lesion.
CSF
• Leukocytosis in bacterial meningitis, cerebral abscess; eosinophils in helminthic (neurocysticercosis) infection; low glucose in bacterial, TB infection; oligoclonal bands of IgG in MS; and cytology to detect malignant cells.
Serum Electrolytes
• Hyperkalemia or hypokalemia in familial periodic paralysis
• In patients with hypokalemia, serum potassium level decreases during attacks, but not necessarily below normal
• In patients with hyperkalemia, serum potassium level may increase to as high as 5-6 mEq/l. Sometimes, it may be at the upper limit of normal, and it seldom reaches cardiotoxic levels.
Muscle Enzymes
• Increased levels of various muscle enzymes such as CK, AST (e.g. muscular dystrophy, polymyositis: vide infra↓↓); in the presence of polymyositis, CK levels can be elevated as much as 50 times the reference level.
TFTs
• Proximal myopathy is known to occur in hyperthyroidism, and cerebellar ataxia may be seen in hypothyroidism.
RA factor and ANA
• In autoimmune arthropathies.
Serum B12 and Folate Levels
• As indicated in megaloblastic anemia.
EMG/NCS
• May be informative in inherited peripheral neuropathy (Friedreich’s ataxia : vide infra ↓↓, Charcot-Marie-Tooth disease) or myopathy.
Genetic Testing
• DNA testing for inherited neuropathies, Friedreich’s ataxia (FA), and muscular dystrophy.
Drug Screen
• Especially for anticonvulsant medications.
Blood alcohol levels if intoxication is suggested.
Muscle Biopsy
• In muscular dystrophy, polymyositis, and connective tissue disease.
CLINICAL NOTES
• Gait abnormality can indicate a serious medical emergency, especially when the problem is associated with any of these additional symptoms:
Headache (raised ICP)
Nausea or vomiting
Decreased alertness
Impaired coordination on only one side of the body
Recent viral illness/immunization (Guillain-Barré syndrome)
Trauma.
A vascular or any lesion causing increased ICP, such as an abscess or a tumor needs to
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be urgently treated. It is therefore important to note the mode of onset and progress
• The presence of associated symptoms and signs such as:
Tinnitus, deafness, or vertigo suggests Ménière’s disease, labyrinthine disease, or eighth nerve lesion;
Headache, nystagmus, or papilledema suggest a cerebellar tumor or acoustic neuroma; and
Glove and stocking anesthesia with diminished reflexes suggest peripheral neuropathy or tabes dorsalis.
• Acute onset hemiplegic gait with symptoms of raised ICP is mostly due to contralateral stroke or head injury. Acute ataxic gait with cerebellar signs (hypotonia, slurred speech, and nystagmus) may be due insufficiency/
thrombosis of to basilar artery/posterior inferior cerebellar artery; drug toxicity;
alcohol abuse; or cerebellar hemorrhage
• Chronic gait disorders are usually due to CNS/spinal mass lesion, infection, nutrit-ional deficiency, substance abuse, or autoim-mune disease such as MS
• Medications, e.g. diuretics, statins, steroids are known to cause myopathies leading to progressive weakness and wasting of skeletal muscles, thus resulting in gait disorders.
Drugs such as antiepileptics (particularly phenytoin and carbamazepine), antihista-mines, benzodiazepines, sedatives-hypnotics, antidepressants, neuroleptics, alcohol, chemotherapy, heavy metal poisoning (e.g.
lead, mercury, and thallium), and bromide intoxication are common and reversible causes of gait disorders
• A careful family history should be obtained to determine if an inheritance pattern can be found. Many types of gait disorders are hereditary, e.g. autosomal recessive ataxias
such as Friedreich ataxia, ataxia telangiec-tasia; and autosomal dominant ataxias such as spinocerebellar ataxia, episodic ataxia, etc.) It is therefore important to look for subtle symptoms in family members. Eliciting information by asking questions such as — are there relatives with clumsiness, frequent falling, late walking, early speech therapy, unusual eye movements, deafness, poor handwriting, or other neurological problems, tendency to diabetes mellitus or mali-gnancies—are very helpful to trace the hereditary etiology and genetic pattern
• Observing the patient stand and walk across the room and carefully observing his posture, gait initiation, base width, step rhythmicity, step length, and arm swing may indicate the likely causative lesion (Table 21.1)
• Tandem walk: Ask the patient to walk a straight line in tandem, i.e. heel to toe. This may reveal a gait abnormality not previously obvious. It also exacerbates all existing gait disorders, especially associated with vestibular and cerebellar disease. Patients with cerebellar disease (e.g. midline cerebellar vermis lesion) will tend to fall preferentially to the side of the lesion
• Ask the patient to walk on his heels. This can not be done by patients with distal muscle weakness or foot drop (L4 or L5 lesion)
• Ask the patient to walk on his toes. This can not be done by patients with Parkinson’s disease, cerebellar disease, or marked soleus or gastrocnemius muscles (S1 lesion)
• A thorough gait assessment should be performed in all older people. An abnormal gait may suggest a remediable risk factor for falls, e.g. difficulty in getting out of a chair without arm support and initiate movement suggests Parkinson’s disease or limb-girdle dystrophy. The ‘Timed Up and Go’ (TUG) test,
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Table 21.1: Common gait disorders
Gait Pattern Cause
Essential Senile gait
Hemiplegic
Paraparetic (Scissor; wooden soldier)
Cerebellar (drunken sailor)
Antalgic
Stamping (sensory)
Steppage
Festinating (propulsive or retropulsive)
Unsteady; careful; slow; short steps;
wide base; stooped posture; diminished arm swing; no rigidity
Extended leg; arms flexed; circum-duction (i.e. round and forward movement)of the affected leg Stiffness (spasticity) of both legs; feet remain on ground
Wide-based; dysmetria; (reeling, unsteady, staggering towards lesion) Limping; avoidance of bearing full weight on the affected leg; limitation of range of movement due to pain in the extremity
High stepping; wide-base; bangs feet down (stamps) clumsily; tends to look at them throughout the cycle (loss of position sense); positive Romberg’s sign Foot drop; high lift to avoid tripping;
slaps on floor; unilateral or bilateral
Rigidity; shuffling (short accelerating steps when walking); festination with stopped posture
Wide-based; hips tilted alternately (glutei weak); waddling or rolling from side to side; toe-walk; lumbar lordosis;
symmetrical
Unsteady; falling to one side; postural imbalance; vertigo; nausea; nystagmus Different, dramatic verities; rare fall or injury; Hoover sign positive
Lack of motor coordination which leaves the patient unable to stand or walk unassisted but normal leg movements can be done when in a sitting or lying down position.
Age-related without accompanying neuropsychiatric abnormality; diffuse cerebral cortex dysfunction; multi-infract dementia
Stroke
Cerebral palsy; cord compression; MS;
syringomyelia
Cerebellar lesion; alcoholism; myxe-dema; MS
OA of the hip or knee; herniated disk;
fracture of any of the bones of the limb;
sprained ankle
Peripheral neuropathy (diabetes mellitus); posterior column lesions, (B12 deficiency-subacute combined degeneration of the spinal cord, HIV myelopathy); tabes dorsalis
Lateral popliteal nerve palsy; peroneal muscular atrophy; cauda equina tumor; Guillain-Barré syndrome;
poliomy-elitis; lead intoxication Parkinson’s disease
Proximal myopathy (muscular dyst-rophy, polymyositis, dermatomyo-sitis); congenital dislocation of the hips; old polio
BPPV; vestibular neuronitis; Ménière’s disease; acoustic neuroma
Conversion disorders
Conversion disorders; rarely in children with posterior fossa tumor, e.g. medulloblastoma
in which the patient is asked to stand up from a sitting position without use of hands, walk 10 feet, turn around, walk back, and sit down, is a valid procedure to readily assess gait disorders.2,3 Patients who take less than 10 seconds are usually normal, patients who
take longer than 30 seconds tend to need assistance with many mobility tasks
• Gait disorders worse in the dark are due to lesions of the posterior column, e.g. Friedreich’s ataxia, pernicious anemia, MS, or tabes dorsalis
• Romberg’s test (eyes-open-eyes-closed): Cerebellar
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ataxia can be differentiated from sensory ataxia by Romberg’s test, where removal of the visual input dramatically reduces compensatory ability in sensory ataxia.
Ask the patient to stand in one place with his feet together. If he is able to stand with his eyes open as well as eyes closed, the test is negative, i.e. normal.
If he is able to stand with eyes open, but tends to fall with eyes closed (i.e.
removing visual input), the test is positive. The cause may be posterior spinal column lesions due to tumor, vit B12 deficiency, cervical spondylosis, or tabes dorsalis.
If he is unable to stand with eyes open and feet together, it indicates severe unsteadiness, commonly involving the peripheral and central vestibular system and the cerebellum.
• Fukuda test: Marching in place for 50 steps;
abnormal if patient deviates close to 90° or more, either to left or right. If abnormal, it reflects vestibular disorder
• Hoover sign: It is a maneuver aimed to separate organic from nonorganic lower limb paralysis. The physician takes a position at the foot of the supine patient and places one hand under the heel of the patient’s ‘weak’
leg while pressing down with the other hand on the good leg. Now the patient is asked to attempt to raise the affected ‘weak’ leg. In organic disease, the associated movement causes the unaffected heel to press downward; in hysteria, the associated movement is absent
• The chair test to aid in the diagnosis of psychogenic gait disorders: In this procedure of ‘chair testing’ patient is asked to walk 20-30 feet forward and backward toward the examiner. The patient is then asked to sit in a swivel chair with wheels and to propel the chair forward and backward. Compared with
his walking, the psychogenic patient is found to perform well on the chair test (sitting versus standing), showing improved ability to propel a chair forward than when seated.
By contrast, a normal person performs equally when walking or propelling utilizing the chair.
RED FLAGS
• In the elderly:
Three “Ds” contribute to gait disorder;
viz. drugs, depression, and dementia;
these must be specifically looked for and excluded before any other intervention.
Acute onset gait disorder is likely to be due to acute systemic decompensation, such as MI, stroke, or sepsis; a careful systematic evaluation is indicated to exclude such catastrophic presentations.
It is often not advisable to attribute gait disorder to a single disease because many different conditions (e.g. degenerative joint disease, postural hypotension, and stroke) can present in similar gait abnormalities.
• In a patient with history suggestive of secondary gain and normal neurological examination, except bizarre gait, strongly favors malingering.
SELECTIVE GLOSSARY
Brown-Séquard syndrome—It is associated with injury to the lateral half of the spinal cord (involving interruption of the lateral corticospinal tracts, posterior white column, and lateral spinothalamic tracts), usually as a result of penetrating trauma to the cervical or thoracic spine. Multiple causes of Brown-Séquard syndrome have been described in the literature.
The most common cause remains traumatic injury, often a penetrating mechanism, such as a stab or gunshot wound or a unilateral facet fracture and
Diagnosis: A Symptom-based Approach in Internal Medicine 144
dislocation due to a motor vehicle accident or fall.
The condition is characterized by the following clinical features (which are found below the level of the lesion): contralateral hemisensory anesthesia to pain and temperature, ipsilateral loss of proprioception, and ipsilateral motor paralysis. Tactile sensation is generally spared.
The pure Brown-Séquard syndrome reflecting hemisection of the cord is not often observed. A clinical picture comprising fragments of the syndrome or the hemisection syndrome plus additional symptoms and signs, known as
‘Brown-Séquard–plus syndrome’, is more common.4 In the absence of trauma, this condition needs to be differentiated from acute poliomyelitis, Guillain-Barré syndrome, cervical disk disease, vertebral artery dissection, infection and inflammatory causes. MRI is helpful to define the extent of spinal cord injury and is also helpful when differentiating among nontraumatic etiologies. CT myelography may be useful if MRI is contraindicated or not available.
‘Fear of falling’ gait—It is largely a psychogenic gait disorder of the elderly that is often unrecognized. It usually begins after a fall and is characterized by a shuffling or sliding stride and an intense need to hold on for support. It appears to be most common in elderly women, can be reversed by education, suggestion, and physical therapy, and is often mistaken for Parkinson disease, or other gait disorders in the elderly.
Friedreich’s ataxia—FA is the most common autosomal recessive ataxia; the major pathophysiologic finding in FA is a “dying back phenomena” of axons, beginning in the periphery with ultimate loss of neurons and a secondary gliosis. Classic FA is the result of a gene mutation at the centromeric region of chromosome 9 (9q13-21.1) at the site of the gene encoding for the 210-aminoacid protein frataxin. Onset of FA is early, with gait ataxia being the usual presenting symptom. Gait ataxia manifests as progressively
slow and clumsy walking, which often begins after normal walking has developed. Diagnostic criteria of typical FA include: disease duration at least 5 years, onset < 25 age, progressive ataxia of gait and limbs, absent knee and ankle jerks, and extensor plantar responses‡. As the disease progresses, ataxia affects the trunk, legs, and arms.
As the arms become grossly ataxic, both action and intention tremors may develop. Eventually, the patient is unable to walk because of the progressive weakness and ataxia, becoming wheelchair bound and ultimately bedridden.
With disease progression, dysarthria and dysphagia appear, incapacitating the patient by 20, and death by 25 (40 in autosomal dominant form), especially due to cardiac failure.
Normal pressure hydrocephalus (NPH)—It is characterized by Adam’s triad (impaired gait, urinary incontinence and dementia) — and an anatomic abnormality, i.e. enlargement of the cerebral ventricles, which can be seen on CT or MRI of brain. The gait is typically wide-based with reduced step height, stride length, and velocity, which gradually progresses to so-called
‘magnetic’ gait (‘feet stuck to ground’ – due to simultaneous contraction of opposing muscles while walking), it becomes almost impossible for the patient to initiate gait. The urinary incontinence is of ‘urge’ type. The precise pathogenesis of NPH is not known, but it is well-known that despite the absence of increased intracranial pressure, the drainage of CSF regularly induces transient clinical improvement, and ventriculosystemic shunting usually results in prolonged remissions. Recently, another anatomic abnormality was described in NPH—
a decrease in midbrain diameter on MRI that is restored to normal by ventriculosystemic shunting. The criteria to define cerebral
‡Only diseases with decreased deep tendon reflexes and positive Babinski signs are Friedreich’s ataxia, amyotrophic lateral sclerosis, B12 deficiency and syphilis.
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ventriculomegaly precisely are vague and difficult to establish, and enlarged ventricles are surprisingly common. Other disorders of elderly people such as Alzheimer’s disease, Parkinson’s disease, and cerebral atrophy may show enlarged ventricles, and demential disorders may be difficult to differentiate from each other.
Polymyositis—It is an idiopathic inflammatory myopathy with symmetric proximal muscle weakness, characterized by subacute or slowly progressing symmetrical weakness, primarily affecting the proximal limb and trunk muscles.
The illness may occur at any age, but is most frequent in the fourth to sixth decade of life, women being more frequently affected than men. Although the initial inciting agent remains unknown, possibilities include virus-mediated muscle injury, e.g. Coxsackie virus B1, HIV, Human T-lymphotropic virus 1 (HTLV-1) Hepatitis B, influenza, echovirus, and adenovirus.
Many drugs are known to cause myopathy, e.g.
hydroxychloroquine, D-penicillamine, hyd-ralazine, procainamide, phenytoin, ACE inhibitors, and statins. Patients may report muscle pain and tenderness, arthralgias or arthritis that may be confused with polymyalgia
rheumatica. Later symmetric proximal muscle weakness in the upper and lower extremities develops. Weakness of pharyngeal and laryngeal muscles, interstitial lung disease, and inflam-mation of the myocardium may also occur. Serum CK levels are usually elevated from 5-50 times the normal value. Other muscle enzymes — lactic dehydrogenase, aspartate aminotransferase, alanine aminotransferase, and aldolase — may be elevated. Muscle biopsy is crucial in helping diagnose PM and in excluding other rare muscle diseases. MRI can be used to guide the site of biopsy.
REFERENCES
1. KurlanR.”Fear of falling” gait: A potentially reversible psychogenic gait disorder. Cogn Behav Neurol 2005;18(3):171-2. [PMID: 16175021:
Abstract].
2. Podsiadlo D, et al. The timed “Up & Go”: A test of basic functional mobility for frail elderly persons.
J Am Geriatr Soc 1991; 39(2):142-8. [PMID: 1991946:
Abstract].
3. Morris S, et al. Reliability of measurements obtained with the Timed “Up & Go” test in people with Parkinson disease. Phys Ther 2001;81(2):810-8. [PMID: 11175678: Free full text].
4. Koehler PJ, et al.The Brown-Séquard syndrome.
True or false? Arch Neurol 1986;43(9):921-4. [PMID:
3741208: Abstract].
SYNOPSIS
Gastrointestinal (GI) bleeding includes bleeding from both upper and lower GI tract.
The upper GI (UGI) bleeding is defined as