EM guidemap - Gait disorders, drop attacks and frequent falls
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Introduction

Clinical evaluation of a gait disorder

Appendix
Introduction

- this guidemap is a companion guidemap to the ataxia, incoordination and dysequilirium guidemap, and it may prove useful if an ataxic patient does not have definite clinical signs of cerebellar disease, acute vestibular syndrome or sensory ataxia; and an emergency physician is seeking guidance on how to r/o other causes of ataxia or disordered gait

- this guidemap is not comprehensive and it does not deal with gait disorders in depth; it is only focused on supplying enough information to allow an emergency physician to recognize some gait disorders due to underlying neurological disease

- there are many reasons why an elderly patient may fall, which are unrelated to a neurological disorder, and this guidemap does not discuss those factors

- it is usually possible to establish a topographic diagnosis (site of the lesion) in a patient with a neurological gait disorder, on the basis of a formal neurological examination and observation of the patient's gait

- the recommended gait evaluation should include the following elements, in addition to a formal neurologic and musculoskeletal examination

Clinical evaluation of a gait disorder

- the clinical evaluation should be focused on identifying some common gait disorder patterns - cerebellar ataxia, vestibular ataxia, sensory ataxia, parkinsonian (akinetic rigid) ataxia, frontal lobe ataxia,and spastic paraplegic ataxia

- after first completing a thorough neurological examination, the clinical approach to an ataxic patient involves an assessment of the patient's standing posture (trunk, stance, postural reflexes) and walking ability (initiation, stepping, associated truncal and upper limb movement)

Standing posture

Trunk posture

- normal subjects stand and walk with an upright posture

- in Parkinson's disease the trunk becomes stooped and flexed and the neck is flexed; neck hyperextension in a Parkinsonian patient suggests other akinetic-rigid syndromes eg. progressive supranuclear palsy syndrome

- a variety of distorted body postures suggest torsion dystonia

- proximal hip muscles weakness, due to a myopathy, causes an exaggerated lordosis

Stance

- assess the patient's stance width, body sway, and ability to balance on two legs during quiet standing

- wide-based gaits suggest a cerebellar or sensory ataxia, diffuse cerebral disease, and frontal lobe lesions; those patients have difficulty standing on one foot or standing with both feet close together

(* a patient who can stand on one foot, with the eyes closed, is unlikely to have objective evidence of a postural balance problem)

- a shaky tremulous stance is seen in Parkinson's disease

- subtle degrees of imbalance can be unmasked by instructing the patient to deliberatedly adopt a narrow stance width when standing, and by watching the patient tandem walk heel-to-toe in a straight line, which tests lateral stability (significantly impaired in cerebellar ataxia)

- because vision is crucial for maintenance of balance in patients with sensory ataxia, instruct the patient to close his eyes during quiet standing (Romberg's test) => the patient with sensory ataxia will sway to the point of falling as unsteadiness dramatically increases

(* see the appendix for further information on Romberg's test)

Postural reflexes

- these reflexes can be tested by gently pushing the standing patient backwards or forwards

- mildly impaired postural reflexes is suggested if the patient takes a few short shuffling steps backwards (retropulsion) or forwards (propulsion), while severely impaired postural reflexes will cause the patient to fall

Walking

Initiation

- start hesitation with shuffling on the spot ("slipping clutch" phenomenon) or an inability to lift the feet from the floor ("magnetic feet" or "stuck-to-the-floor" phenomenon) are signs of difficulty initiating gait, and start hesitation (freezing of gait) is usually seen in extrapyramidal syndromes, frontal lobe lesions, and rarely as an isolated condition (gait ignition failure)

- freezing of gait is a midline phenomenon and usually involves both legs, but in asymmetric Parkinsonism unilateral or asymmetric freezing can occur

- freezing of gait (FOG) is often worse in stressful situations eg. answering a doorbell, crossing a street at a green light

- one of the classical features of FOG is its dramatic and continuous response to motor or behavioural tricks eg. moderate emotional distress may improve FOG (level of function better in the doctor' office compared to level of function at home, where FOG is at its worst)

Stepping

- when walking is underway, assess the patient's stride length, rhythm and speed of walking over a distance of 5 - 10 metres, and note his ability to quickly turn around and negotiate obstructions

- in parkinsonian syndromes, the length of each step is short, and steps may be slow and shallow, although the normal rhythm of walking is maintained

- in cerebellar ataxia, the steps are of variable length and irregular in rhythm, giving the gait a jerky and lurching quality, which is exacerbated when the patient needs to turn corners => the patient's walk may take a zig-zag course mimicing a drunken sailor; there may also be titubation and swaying of the head and trunk; widening of the base only during turns or merely taking an extra one-or-two steps during sudden turns to maintain balance + slight difficulty with tandem walking may be the earliest signs of cerebellar ataxia

- the pattern of cerebellar ataxia depends on the site of the pathology => lesions of the flocculonodular lobe (vestibulocerebellum) may produce marked dysequilibrium causing postural ataxia during sitting or standing + severe gait ataxia and falling in any direction +/- truncal titubation when sitting or standing + few/no other cerebellar signs; lesions of the anterior vermis (spinocerebellum) may produce a wide-based gait with a slow and irregular cadence and superimposed lurching, but no/few other signs of incoordination; lesions of the lateral cerebellar hemispheres (frontocerebellum) mainly produce limb ataxia and secondary gait incoordination with a tendency to veer towards the ipsilateral side + multiple associated cerebellar hemisphere signs, but no true truncal ataxia

- in sensory ataxia, the steps are slow and deliberate and placed carefully under direct visual guidance, sometimes striking the ground with the heel then the foot, making a slapping sound (slapping gait); gait is much more impaired when walking in the dark and the feet may be raised too high, thrown too far forward and brought down too hard; the patient shows poor/absent postural responses to surface perturbations even with the eyes open

- in vestibular ataxia due to bilateral peripheral vestibular dysfunction, the patient may have normal gait under usual circumstances, but have significantly impaired gait when vision and proprioceptive cues are reduced or deceptive eg. walking in the dark or over uneven ground; the patient may try and keep the head still while walking to prevent oscillopsia and secondary dysequilibrium (stiff "en bloc" gait)

- in vestibular ataxia due to unilateral peripheral vestibular dysfunction, the patient often has marked vertigo and secondary autonomic symptoms during the acute phase and is disinclined to walk; if coaxed to walk the patient tends to fall or stagger towards the affected side (opposite in direction to the subjective sense of self-motion and the rapid phase of nystagmus); balance is much better when running versus slow walking

- in upper motor neuron disease, the patient stands with slight flexion at the hips and knees, but on starting to walk, the leg stiffens and extends slightly at the knee; most of the lower limb movement comes from the hip and walking involves circumduction of the stiffened leg during the swing phase of each step, with scraping of the toes of the shoe on the ground beneath as the trunk undergoes slight flexion to the opposite side to allow the hyperextended leg to swing through; severe thigh adductor spasm may even cause the the circumducted leg to cross the midline during the swing phase producing a scissoring gait

(* the characteristic clinical picture of a spastic hemiparesis includes the arm posture of abduction and internal rotation of the shoulder, pronation of the forearm and flexion of the wrist and fingers, with a minimum of associated arm swing on the affected side; in spastic paraparesis there is slight flexion at the hips, both legs are extended at the knees, and the feet adopt a posture of plantar flexion => gait is slow as the patient proceeds by dragging the circumducted legs forward, one step after another; the most common cause of a spastic paraplegia in an elderly patient is a spinal myelopathy due to cervical spondylosis; patients with hereditary spastic paraplegia or cerebral palsy have only minor increases in motor tone when examined supine, but they have profound leg spasticity when walking)

(* see the spinal cord syndromes guidemap for futher problem-solving information on UMN motor and sensory signs)

- in lower motor neuron disease involving the proximal hip and pelvic muscles, weakness of the hip extensors leads to an exaggerated lordosis; flexion of the hips and a failure to stabilize the pelvis during walking => leads to an exaggerated pelvic tilt and a waddling gait

- in distal lower motor neuron weakness causing foot drop, the legs are lifted abnormally high with each step, descending to strike the floor with the toes first and then the heel (steppage gait)

- dystonic syndromes may produce bizarre gait abnormalities, which can lead to a misdiagnosis of psychogenic gait disorder

- patients with chorea often incorporate the involuntary movements into their gait, describing an irregular path with a dance-like pattern likened to a "puppet-on-a-string"

Associated movements

- normal subjects walk with flowing synergistic movements of the head, trunk and arms

- loss of synergistic arm movements is seen in akinetic-rigid syndromes, hemiparesis, spastic paresis and cerebellar ataxia

- an unilateral loss of arm swing may be an early sign of a hemiparesis or Parkinson's disease

Basal ganglia gait disorders

- the major deficit in early Parkinson's disease is a reduction in the speed and amplitude of leg movements, giving rise to a shuffling gait with small steps and no/little raising of the feet during walking (the foot is placed flat or plantarflexed during walking)

- the locomotor hypokinesia is associated with diminished arm swinging, and the body turns "en bloc" (head remains in line with the body during turning)

- as the disease progresses, freezing develops and the patient develops start hesitation (referred to as "magnetic" feet) => the patient shuffles on the spot or the feet appear stuck to the floor

- after walking starts, freezing may recur when the patient turns or enters a doorway or encounters an obstacle

- balance and postural reflexes are preserved in the early stages, although the response to a disturbance of posture is a series of short shuffling steps (propulsion, retropulsion, festination)

- postural instability and falling appear later in the disease course

- patients with other akinetic-rigid (Parkinson's plus) syndromes are more likely to have a wide-based gait, absent/poor postural reflexes and frequent falls

(* see the table differentiating Parkinson's disease from other akinetic-rigid syndromes)

It should be possible - based on the formal neurological examination + observation of standing posture and gait - to decide whether the patient has a lower-level or middle-level gait disorder

(* see the classification of gait disorders for a list of causes of gait disorders)

If the neurological examination and observation of the ataxic gait does not suggest a lower-middle-level gait disorder, consult the following brief synopses of different higher-level gait disorders for further problem-solving information

Higher-level gait disorders

Cautious gait (senile gait)

- many elderly people adopt this gait to compensate for arthritis or in response to frequent previous falls

- the patient appears to be adopting too many unnecessary precautions as if "walking on ice" - the feet are placed wide apart; the body and hips and knees are flexed to place the body directly over the widened base; the arms are held abducted and flexed in anticipation of an unexpected  fall; walking proceeds with small tentative steps on a wide base and the patient frequently reaches out for furniture or other objects for support

- some elderly patients develop space phobia and only walk timidly around the periphery of the room

Subcortical dysequilibrium (astasia-abasia, thalamic astasia)

- astasia is motor incoordination and an inability to stand, abasia is an inability to walk

- secondary to thalamic or midbrain stroke; also seen early in the course of progressive Parkinson's-plus syndromes

- the patient has normal muscle strength on isometric testing and variable sensory loss

- the patient may be unable to stand because of an absence of postural reflexes, or the patient may fall over easily

- postural reflexes may also be inappropriate and the patient may extend the neck and fall backwards or sideways immediately on standing; extreme cases cannot even sit up unassisted

- if the patient can ambulate, the patient may have particular difficulty walking backwards and the patient needs to pay particular attention in order to walk satisfactorily

- associated neurological defects include vertical gaze palsies, dysarthria and extrapyramidal signs (proximal hypokinesia, and poverty in the performance of associated automatic movements)

Frontal dysequilibrium (frontal ataxia, gait apraxia)

- associated with frontal lobe disorders (tumor, abscess, infarction or normal pressure hydrocephalus)

- patients have difficulty in rising to stand upright because they do not bring their feet under themselves as they try to rise, and they may not even place their feet on the ground

- if helped to stand erect, they often arch back into hyperextension in seeming disregard for their support base

- there is often a complete breakdown in the organization of leg movements and the legs may scissors-cross in bizarre gait patterns, and there is no coordination between the trunk and legs

- can be distinguished from subcortical dysequilibrium because those patients can walk once locomotion starts and a few steps have been taken, while patients with frontal dysequilibrium remain completely uncoordinated and cannot ambulate

- associated with frontal dementia, urinary incontinence, frontal release signs and perseveration

Isolated gait ignition failure (gait apraxia, magnetic gait)

- characterized by an inability to initiate locomotion

- the patient may appear to be frozen to the spot on gait initiation, or when required to turn

- balance is preserved, postural responses are normal, gait width is normal and falls are very rare

- steps are initially short and shuffling, but become more normal as walking proceeds, and the arm swing also  becomes normal when the patient eventually ambulates

- there are no physical signs of Parkinsonism or dementia

- the cause is unknown, and neuroimaging is required to r/o hydrocephalus or multi-infarct disease (both conditions are usually  associated with dementia and urinary incontinence)

Frontal gait disorder (arteriosclerotic Parkinsonism, lower half Parkinsonism)

- seen in the multi-infarct state due to subcortical hypertensive arteriosclerotic encephalopathy (Binswanger's disease) and hydrocephalus

- the patient has a normal-wide base, stiff upright stance when standing and walking, difficulty initiating ambulation, short-stepped military gait with exaggerated arm movements, hesitation on turning, and freezing episodes

- there is some impairment of postural reflexes and a variable tendency to fall

- associated with cognitive impairment, pseudobulbar palsy, dysarthria, urinary incontinence, frontal release signs and pyramidal signs (UMN signs)

- no signs of Parkinson's disease (rest tremor, facial immobility, reduced upper arm movements, bradykinesia)

Psychogenic gait disorder

- psychiatric findings are heterogenous and some patients have depression while other patients have conversion hysteria disorder

- clinical features suggestive of psychogenic gait ataxia

Summary of the clinical differences between major ataxic conditions causing a wide based gait
  Cerebellar ataxia Sensory ataxia Frontal lobe ataxia
Trunk posture Stooped-leans forward Stooped-upright Upright
Stance Wide-based Wide-based Wide-based
Initiation of gait Normal Normal-wariness Start hesitation
Postural reflexes +/- Intact May be absent
Steps Stagger-lurching High-stepping Small-shuffling
Stride length Irregular Regular Short
Leg movement Variable, ataxic Variable - hesitant and slow Stiff, rigid
Speed of movement Normal-slow Normal-slow Very slow
Arm swing Normal, exaggerated Normal Exaggerated
Turning corners Veers away Minimal effect Freezing-shuffling
Heel-toe test Unable +/- Unable
Romberg's test +/- Increased unsteadiness +/-
Heel-shin test Usually abnormal +/- Normal
Falls Uncommon Yes Very common

 
Differentiating between Parkinson's disease and symptomatic Parkinsonism in akinetic-rigid syndromes
  Parkinson's disease Symptomatic parkinsonism
Posture Stooped (trunk flexion) Stooped/upright (trunk flexion or extension)
Stance Narrow Often wide-based
Postural reflexes Preserved in early stages Absent at early stage
Initiation of walking Start hesitation Start hesitation
Steps Small and shuffling Small and shuffling
Freezing Common Common
Festination Common Rare
Arm swing Reduced-absent Reduced
Heel-toe walking Normal Poor
Falls Late (forwards-tripping) Early and severe (backwards)

Drop attacks and frequent falls

A drop attack is defined as a sudden fall, with or without loss of consciousness, due either to collapse of muscle tone (a negative phenomenon) or abnormal muscle contraction in the legs (a positive phenomenon)

(* some physicians exclude any patients with loss of consciousness from the category of drop attacks)

- about two-thirds of drop attacks of are of unknown etiology

- many neurological and cardiac diseases can cause drop attacks, and a brief discussion of some causes of drop attacks follows:-

Proximal weakness of the legs

- some causes include muscular dystrophy, neurogenic atrophy, polymyositis, inclusion body myositis, myasthenia gravis and spinal cord ischemic attacks

- Duchenne's muscular dystrophy is the most common muscle dystrophy to cause weakness of the hip and knee extensors, which are important for maintaining an erect posture

- rarely, middle-aged patients may  develop drop attacks due to isolated quadriceps weakness, secondary to diseases like polymyositis, inclusion body myositis and neurogenic atrophy, and the legs may suddenly give way without warning to cause falls

- intermittent spinal ischemia can produce sudden attacks of transient paraparesis or falls, and causes include syphilitic arteritis, arteriosclerosis of the distal aorta, adhesive arcachnoiditis, spinal compression due to spinal stenosis or disc herniation; the attacks are often precipitated by exercise and relieved by rest

Neurodegenerative diseases

- patients with Parkinson's disease often fall due to defective postural reflexes, sudden freezing, and uncoordinated turning; their stooped flexed posture predisposes them to falling forward because their centre of gravity is displaced forward when standing or walking; drug-induced dyskinesias and orthostatic hypotension can also predispose them to falls

- patients with Parkinon's plus syndromes (other akinetic-rigid disorders) are more prone to fall

- falling is the most frequent initial presenting symptom in progressive supranuclear palsy, and PSP patients tend to extend their necks and fall backwards; stiff legs + wide-based gait + absent postural reflexes + characteristic down-gaze palsy predisposes PSP patients to frequent falls

- other neurodegenerative diseases associated with frequent falls include corticobasal degeneration, Huntingdon's chorea, multiple system atrophy and Alzheimer's disease

Transient ischemic attacks

- the patient with vertebro-basilar artery ischemia can present with a sudden loss of tone in their legs, causing their knees to buckle => the patient falls powerlessly without protective arm movements; there may be no precipitating head or neck movements or loss of consciousness, and the patient can ususally get up and walk immediately or within one minute; usually other symptoms of brainstem ischemia are present (vertigo, diplopia, bluured vision, sensory changes, motor weakness and variable LOC), which suggest the diagnosis

Epilepsy

- drop attacks can be due to sudden muscle contractions associated with generalized convulsive epilepsy, or a sudden loss of postural tone due to atonic epilepsy or epileptic negative myoclonus

- the Lennox-Gastaut syndrome consists of a variable mixture of myoclonic, atonic, tonic and abscence seizures; these patients have a past history of brain damage and mental retardation, and seizures occur between 6 months and 7 years

- atonic epileptic attacks in children can occur when standing or sitting or lying, and there is no aura or postictal state of confusion; sudden drop attacks can cause the patient to collapse like an accordion with triple flexion of the legs and no involvement of the arms => the patient can usually get up immediately after an attack

Various myoclonic syndromes

- mycoclonus is defined as a sudden brief, shock-like muscle movement caused by a brief muscle contraction (positive myoclonus) or inhibition of a muscle contraction (negative myoclonus)

- they can mimic idiopathic drop attacks, and the patient can fall suddenly with buckling of the legs

- many patients exhibit repetitive bouncing of the legs when they attempt to stand, due to repetitive negative myoclonus in the extensor support muscles of the trunk and hips

Startle reactions

- pathological startle reactions (hyperekplexia) are characterized by an exaggerated motor response to unexpected auditory stimuli, and less frequently to visual or somasthetic stimuli

- pathologic startle reactions consist of both brief myoclonic jerks and longer tonic spasms

- hyperekplexia may have a variety of causes eg. idiopathic, hereditary, or secondary to acquired brainstem diseases - post-anoxic encephalopathy, viral or paraneoplastic brainstem encephalitis, multiple sclerosis, sarcoidosis or brainstem strokes

- myoclonic jerks occur frequently during the day, but also at night when the patient is asleep, and mainly affect the legs

- sterotyped tonic spasms consist of facial grimacing, flexion of the neck and trunk, flexion or extension of the hips and knees, and characteristic abduction of the shoulders with flexion of the elbows => the patient falls forwards rigidly like a log, but sometimes falls backwards; protective reflexes are impossible and injuries common; consciousness in maintained during the fall and recovery is fast

Cataplexy and paroxysmal kinesigenic choreoathetosis

- cataplexy can cause sudden falls without LOC, but the patient cannot speak during the fall

- characteristic precipitating factors include laughter or a sudden emotional stimulus

- minor symptoms of cataplexy may consist of a brief drop of the jaw and sagging of the head, but severe attacks can cause loss of tone in all the antigravity muscles => the patient falls powerlessly and loosely and remains immobile for many seconds (longer than in hyperekplexia)

- attacks of paroxysmal kinesigenic choreoathetosis are usually precipitated by sudden leg movements during standing or running or social embarrassment => the patient may suddenly lose control due to tonic spasms or an involuntary choreoathetotic muscle movement and fall like a log

Focal structural lesions

- mass lesions around the foramen magnum can cause drop attacks (eg. odontoid process fractures, Arnold-Chiari type I malformations), and drop attacks can be precipitated by neck movements, coughing or sneezing, or vertical head compression; the drop attack patient presents with a stiff  neck, spastic paraplegia. Lhermitte's sign and limb paresthesias

- other posterior fossa pathology can also cause drop attacks eg. posterior fossa arachnoid cysts, midline metastatic cerebellar tumors, vermis hemangioblastomas, and obstructive hydrocephalus due to third ventricle cysts

Meniere's drop attacks (Tumarkin's otolithic crisis)

- seen in the early or late stages of Meniere's disease when there is a sudden change in endolymphatic pressure which causes end-organ stimulation with a reflex-like vestibulospinal loss of postural tone

- the patient suddenly loses control of balance and falls; the patient does not lose consciousness and he sometimes has the distinct feeling of being pushed or thrown to the ground

(* a patient with Wallenberg's syndrome, due to a lateral medullary stroke, may have a similar transient sensation of being pulled or pushed to the side, and the patient suddenly falls to the side without realizing that it is his active shift of the centre of gravity - lateropulsion - that causes the momentary imbalance)

Idiopathic drop attacks

- proposed diagnostic criteria include:- "A fall without warning, not associated with loss of consciousness, not apparently due to any malfunction of the legs, not induced by changes of posture or movement of the head, and not accompanied by vertigo or other cephalic sensation, and not associated with myoclonic jerks"

- usually appear between the ages 40 - 60 years

- patients only fall when standing or walking, and they usually buckle at the knees and fall forwards

- the attacks occur very suddenly and the patient cannot remember if he lost consciousness, or not; the patient can get up immediately unless accidental injury occurs (minor upper limb fractures and/or dislocations are common in the elderly)

- serial attacks are rare, and spontaneous remission is common (25 - 80%)
 
Appendix

Classification of gait disorders

Lowest-level gait disorders

Peripheral musculoskeletal problems

Peripheral sensory problems Middle-level gait disorders Higher-level gait disorders Romberg's test

- the test is primarily used to differentiate sensory ataxia from cerebellar ataxia

- Romberg's sign detects proprioceptive sensory loss by demonstrating loss of postural control in darkness

- the test is usually performed by having an examiner observing the patient's postural stability when the patient stands with the feet close together, initially with eyes open and then with eyes closed

- Romberg's sign is present when a patient is able to stand with feet together and eyes open, but sways or falls with the eyes closed

(* normal people may sway a little when the eyes are closed, and a Romberg test is only truly positive when the patient sways a great deal or falls)

- the test is classically positive in patients with proprioceptive loss (due to dorsal column disease or peripheral sensory neuropathy) because they are dependent on visual cues to remain in a state of postural equilibrium; however, patients with bilateral vestibular damage are also dependent on visual cues for balance and they may also have a positive Romberg's sign

- some patients* with cerebellar ataxia also have a positive Romberg's sign and they are also dependent on visual cues for maintenance of postural balance while standing

(* the pathology lies in the anterior vermis and paravermis of the anterior lobe - spincocerebellum - and is commonly due to alcohol damage; the patient has an anterior-posterior sway with a frequency of 3Hz; the patient rarely falls because the body tremor is opposite in phase in head, trunk, and legs, resulting in minimal shift of the center of gravity)

Disclaimer: My EM guidemaps reflect my personal approach to problem-solving/managing clinical cases in an ED setting and they should not be regarded as the standard of care. They merely represent the personal opinions of the author and they should only be used in clinical practice if the reader-user has substantial reason to believe that the clinical advice contained in the guidemaps is valid and accurate. The guidemaps are not meant to be "authoritative" and the reader-user should consult standard medical textbooks and expert opinion articles/guidelines for more authoritative advice. The reader-user should particularly confirm all drug doses, their indications and contra-indications, prior to their use.