Enough is now known about nystagmus to make it a valuable clinical finding, provided that it is characterised systematically, and interpreted in the context of the general neurological evaluation. Nystagmus may be defined as repetitive, to and fro, involuntary eye movements that are initiated by slow drifts. Nystagmus may consist mainly of sinusoidal slow phase oscillations (pendular nystagmus) or, more commonly, of an alternation of slow drift and corrective quick phase (jerk nystagmus). Common waveforms are schematised in figure 1. Thus, each slow phase takes the eye away from the preferred direction of gaze and the corrective quick phase (a saccade) brings the eye back towards the visual target. Although nystagmus is often described by the direction of its quick phases (for example, downbeat nystagmus), it is the slow phase that reflects the underlying disorder. Nystagmus should be differentiated from saccadic intrusions and oscillations, in which rapid movements (saccades) take the eye away from the target (fig 1).
Modern classifications of nystagmus are based on current knowledge of the neurobiology of eye movements,1 and disorders of the three mechanisms that normally hold gaze still (visual fixation, the vestibulo-ocular reflex, and the eccentric gaze holding mechanism).2 However, at the bedside, the clinician must rely on the observed characteristics of nystagmus and a systematic examination of eye movements to deduce the significance of any ocular oscillations. Here we describe how to elicit nystagmus and saccadic oscillations, and then summarise the general significance of common forms of nystagmus. To realise the full diagnostic value of nystagmus requires a broader discussion of pathophysiology, which can be found in standard neuro-ophthalmological textbooks.2–4 Some brief video examples of common forms of nystagmus have been posted at the journal web site, and others are available in a text/CD.2
Inquire about the duration of the nystagmus, whether it interferes with vision or causes oscillopsia (illusory motion of the visual world), and whether it is accompanied by other neurological symptoms. In general, oscillopsia is a feature of acquired, not congenital, nystagmus. Ask if associated visual symptoms are worse when viewing far or near objects, during specific directions of gaze (for example, downgaze), or when the patient is in motion (which implies a vestibular disorder). Try to determine if the nystagmus is congenital by asking about “jumping eyes,” strabismus, eye patching, or eye operations since childhood. Check the patient’s current medications for agents with effects on the brain (for example, anticonvulsants). If the patient habitually tilts or turns the head, determine whether these findings are evident on old photographs, which would suggest congenital nystagmus.
Before starting an evaluation of nystagmus, note any abnormality of head posture, examine the visual system (acuity, fields, colour, stereopsis), optic nerves, lids, pupils, and look for signs of ocular albinism. Several congenital forms of nystagmus are associated with disorders of the visual system.2–4
Before examining for nystagmus, determine whether there is a full range of the movements of each eye, and note any static deviation (strabismus). Then observe the stability of gaze as the patient attempts to fix upon a stationary target (such as the letter X) at a viewing distance greater than 2 m. With the patient’s eyes close to central position, determine whether there is any nystagmus. For each eye, note the directions in which the nystagmus occurs: horizontal, vertical, torsional (rotational around the line of sight), or mixed. Compare the nystagmus in each eye, and note whether the direction or size of movement differs, or if there is any asynchrony. If the size of the oscillations differs in each eye, it is referred to as dissociated nystagmus. If the direction of the oscillations in each eye differs, it is called disconjugate or disjunctive nystagmus. Cover each eye in turn to check for latent nystagmus (see video “Latent_Nystagmus”). Some nystagmus is intermittent and requires sustained observation over several minutes. Low amplitude nystagmus may only be detected during ophthalmoscopy5; note that the direction of horizontal or vertical nystagmus is inverted when viewed through the ophthalmoscope. Repeat each of these observations as the eyes are brought into right, left, up, and down gaze, and during sustained convergence.
A description of the direction of rotation of the nystagmus in each gaze angle will often indicate the coordinate system to which the nystagmus conforms. Thus, nystagmus that appears horizontal in the straight ahead position of gaze but torsional on looking far up is rotating around a rostral-caudal axis relative to the head, characteristic of vestibular nystagmus. However, if on upward gaze the nystagmus still appears “horizontal” to the observer, then the eye is rotating around an eye fixed axis, characteristic of congenital nystagmus (see video “Congenital_Nystagmus”).
Always examine the effect on nystagmus of removing fixation; nystagmus attributable to peripheral vestibular imbalance may only be apparent under these circumstances. The best way is to observe the nystagmus behind Frenzel goggles (high positive lenses with small lights), which prevent fixation of objects and also provide the examiner with a magnified, illuminated view of the patient’s eyes. If not available, another technique consists of transiently covering the fixating eye during ophthalmoscopy in an otherwise dark room, and noting the effects on retinal motion in the eye being viewed.5
Evaluation of nystagmus is incomplete without a systematic examination of each functional class of eye movements—vestibular, saccades, smooth pursuit, and vergence; selective defects may indicate the nature of the underlying disorder. For example, dissociated nystagmus (greater in the abducting eye) on looking to the right occurs when the adducting left eye cannot be put on target because of an internuclear ophthalmoplegia. It is also important to note the effects of each type of eye movement (such as convergence) on the nystagmus, as well as a 15 second period of head shaking in the horizontal or vertical planes (observe the nystagmus after head shaking through Frenzel goggles).2,6 Placing the patient into head hanging positions may increase some forms of nystagmus (for example, downbeat). Nystagmus that is present only when induced by positional testing is a feature of benign paroxysmal positional vertigo, which is discussed elsewhere.2,7
It is possible to induce nystagmus in normal subjects with optokinetic or vestibular stimuli. Under natural circumstances, visual (optokinetic) and vestibular nystagmus acts to hold images steadily on the retina during self rotation. In clinical practice, it is convenient to induce nystagmus with an “optokinetic” drum or tape, which presents a moving pattern of stripes. This stimulus mainly tests smooth pursuit tracking (slow phases) and automatic saccades (quick phases). The patient is instructed to follow the stripes as they move either horizontally or vertically. The clinician looks for an asymmetry of responses. For example, with an infarction of right posterior cerebral cortex that affects secondary visual areas concerned with motion processing, the response will be reduced as the stripes move to the patient’s right (impaired ipsilateral smooth pursuit) and less corrective quick phases will be triggered—that is, there will be less nystagmus as the stripes move to the patient’s right compared with moving to the left.
Nystagmus can also be induced with vestibular stimuli.2,7 A simple method is to rotate, by hand, the patient in an office chair for 45 seconds, then stop the chair so that induced nystagmus can be viewed. Vestibular nystagmus can also be induced by irrigating the external auditory canal with cool or warm water, which produces a convection current in the endolymph of the labyrinth. In clinical practice, the minimal ice water caloric test is most convenient.2,8 After verifying that the tympanic membrane is intact, the patient’s head is elevated 30 degrees relative to earth horizontal, to place the lateral semicircular canal in a vertical position. Ideally, eye movements should be observed behind Frenzel goggles. A normal response, consisting of a nystagmus beating away from the stimulated ear, can be elicited with as little as 0.2 ml of ice cold water. The caloric test is a sensitive indicator of loss of unilateral vestibular function.
INTERPRETATION OF FINDINGS
Nystagmus occurring when the eyes are close to central position
An important first step is to determine whether removing visual fixation increases the nystagmus. Mixed horizontal-torsional jerk nystagmus that suppresses with fixation is usually attributable to a peripheral vestibular imbalance and is accompanied by vertigo (for example, viral labyrinthitis).2,7 Peripheral vestibular nystagmus (fig 1A) commonly beats away from the side of lesion, and increases when the eyes are turned in the direction of the quick phases (Alexander’s law). Horizontal nystagmus (jerk or pendular) that is accentuated by the visual effort of fixation, as well as by attention or anxiety, is commonly congenital. Congenital nystagmus usually remains horizontal in all gaze angles, may be suppressed during convergence (see video, “Congenital_Nystagmus”), and is sometimes associated with anomalous head positions, head oscillations and strabismus.4 A characteristic sign of congenital nystagmus is that during testing with a horizontal optokinetic stimulus, the quick phases may be directed in the same direction as drum motion—“optokinetic inversion.” Horizontal nystagmus that changes direction when the eyes are alternatively covered (beating away from the covered eye) is usually “latent nystagmus”, which is associated with lack of normal binocular development (absent stereopsis), and childhood strabismus (see video, “Latent_Nystagmus”).4 Latent nystagmus is often manifest when neither eye is occluded, because the patient chooses to fixate with one eye. These congenital variants of nystagmus are usually evident from the examination and history of lifelong eye problems. However, sometimes it is necessary to record eye movements, because most waveforms of congenital nystagmus are diagnostic, especially increasing velocity waveforms (fig 1C) with superimposed “foveation periods,” when the eyes are momentarily still.4 The diagnostic significance of these congenital forms of nystagmus to the neurologist are that they usually require no further evaluation. Horizontal nystagmus that regularly reverses direction about every two minutes is periodic alternating nystagmus (PAN); it is associated with disease of the midline cerebellum (nodulus and uvula).2 To identify this oscillation, which is usually unaffected by visual fixation, an observation of a few minutes is required, and the examiner should also look for periodic alternating head turns that may be associated. A congenital variant of PAN, which is not related with cerebellar disease, usually does not reverse direction at regular intervals.4
Vertical jerk nystagmus (downbeat or upbeat), as well as purely torsional jerk nystagmus, with the eye near to central position is usually attributable to a central involvement of the vestibular pathways. Both downbeat and upbeat nystagmus are poorly suppressed by visual fixation and may be exacerbated by simply placing the patient in a head hanging position; they may also be increased, suppressed, or inverted by convergence.2 Typically downbeat nystagmus is best evoked on looking down and laterally (see video “Downbeat_Nystagmus”), whereas upbeat nystagmus generally increases on looking up. Downbeat nystagmus is usually encountered with lesions of the vestibulocerebellum, craniocervical anomalies, and drug intoxications; it is also a feature of the calcium channelopathy, episodic ataxia type II.2,9 Upbeat nystagmus is less well localised, being mainly reported with lesions in the medulla,6 or close to the superior cerebellar peduncle (see video “Upbeat_Nystagmus”).2 Pure torsional nystagmus with the eye close to central position is uncommon and is usually associated with medullary lesions, such as syringobulbia and lateral medullary infarction (Wallenberg’s syndrome).2,10 It is often accompanied by ocular tilt reaction or unilateral internuclear ophthalmoplegia.11
Acquired pendular nystagmus has a quasi-sinusoidal waveform (fig 1D),12 and often shows trajectories that are oblique, elliptical, or circular, depending on the size and temporal relation between horizontal and vertical components. Congenital pendular nystagmus is usually horizontal in direction. Acquired pendular nystagmus may be conjugate, disconjugate (dissimilar trajectories of each eye), or dissociated (different size of oscillations in each eye). It occurs most commonly in association with disorders of central myelin, especially multiple sclerosis (see video, “Pendular_Nystagmus”),12,13 and after brain stem stroke as part of the syndrome of oculopalatal tremor (“myoclonus”).2
Pendular oscillations that are about 180° out of phase in the horizontal plane causes a type of convergent-divergent nystagmus, which occurs in some patients with cerebral Whipple’s disease, sometimes with associated oscillatory movements of the jaw, face, or limbs (oculomasticatory myorhythmia) and vertical gaze palsy.14 Pendular convergent-divergent nystagmus has also been reported in patients with multiple sclerosis and brain stem stroke.15 Convergence-divergence nystagmus should be differentiated from conjugate nystagmus that is affected (suppressed, increased, or inverted) by convergence, a feature of a variety of acquired forms of nystagmus (for example, downbeat, upbeat nystagmus). Congenital nystagmus is often suppressed during convergence.4
Seesaw nystagmus (pendular or jerk) consists of elevation and intorsion of one eye and synchronous depression and extorsion of the other eye in the first half cycle, followed by change in direction during the next half cycle. To appreciate the seesaw nature of the oscillation, it often helps to look at the bridge of the patient’s nose. Pendular seesaw nystagmus occurs with disorders that interfere with crossing axons at the optic chiasm and cause bitemporal hemianopia, such as pituitary tumours, as well as a variant of congenital nystagmus (see video “Seesaw_Nystagmus”).4 Jerk seesaw nystagmus is reported in patients with lesions in the region of the interstitial nucleus of Cajal.16
Nystagmus induced by moving the eyes to an eccentric position—gaze evoked nystagmus
The commonest form of nystagmus encountered in clinical practice occurs only when the eyes are moved into eccentric gaze, especially in lateral and up gaze (fig 1B). This gaze evoked nystagmus has quick phases that are directed away from central position (see video, “Gaze&Rebound_Nystagmus). Holding the eyes in such eccentric positions requires a tonic contraction of the extraocular muscles, which is achieved by a sustained discharge of motoneurons.17 This ability is impaired by cerebellar and brainstem disorders as well as a number of intoxications.2 Thus, the finding of nystagmus on lateral or upgaze may be clinically important. Firstly, however, it is important to differentiate between pathological gaze evoked nystagmus and its variant, called end point nystagmus, frequently reported in normal subjects. The latter is usually unsustained, of low frequency and amplitude, and not accompanied by other ocular motor abnormalities. Pathological gaze evoked nystagmus may be attributable to a peripheral process,2 being a sign of extraocular muscle weakness, for example, in patients with myasthenia gravis (“fatigue nystagmus”). It also occurs as a result of central disorders that involve the gaze holding neural network, which includes the nucleus prepositus hypoglossi and medial vestibular nucleus for horizontal gaze,17 the interstitial nucleus of Cajal for vertical gaze,18 and the vestibulocerebellum,2 which optimises gaze holding. Structural lesions affecting this gaze holding network may cause gaze evoked nystagmus, because the eyes tend to drift back to central position (fig 1B). Most commonly, gaze evoked nystagmus is encountered as a side effect of medications, including sedatives and anticonvulsants, or with drug intoxications (for example, alcohol). When patients with gaze evoked nystagmus attempt to hold eccentric gaze for a number of seconds, and then return their eyes to the central position, a transient rebound nystagmus, with quick phases opposite to the direction of the prior eccentric gaze, may occur (see video “Gaze&Rebound_Nystagmus”). Such rebound nystagmus is prominent in patients with disease affecting the vestibular cerebellum.19
When nystagmus on lateral gaze is greater in the abducting eye, the cause may be internuclear ophthalmoplegia, and saccades should be tested, looking for slowing of the adducting eye. In most cases, dissociated nystagmus is a manifestation of the brain’s attempt, with a series of saccades, to put the fovea of the weak, adducting eye on target.2 Tumours of the cerebellopontine angle may cause a combination of low frequency, large amplitude horizontal nystagmus looking ipsilaterally, because of defective gaze holding, and a high frequency, small amplitude nystagmus on looking contralaterally because of vestibular imbalance (Bruns’ nystagmus).
One form of nystagmus induced by upgaze is convergence-retraction nystagmus. It occurs with dorsal midbrain lesions (for example, pineal tumours). Convergence-retraction nystagmus may be elicited either by asking the patient to make an upward saccade, or by using a handheld optokinetic drum or tape, moving the stripes down. In some cases the convergent movements appear to be opposed vergence movements,20 but in others it consists of opposed, asynchronous saccades.21
Nystagmus (either jerk or pendular, binocular or monocular) occurs commonly in patients with visual impairment or loss, who cannot accurately direct their gaze. In such patients, both horizontal and vertical components are present, and the direction of nystagmus fluctuates during a period of observation. Their nystagmus probably reflects an uncalibrated ocular motor system.22
Saccadic intrusions and oscillations
Several types of inappropriate saccadic movements may intrude upon steady fixation; more common variants are schematised in figure 1E–G. Because saccadic intrusions are rapid and brief, it is usually necessary to measure eye and target position and eye velocity to identify accurately the saccadic abnormality.
Square wave jerks (fig 1E) occur in healthy subjects,23 but are a prominent finding in progressive supranuclear palsy and some spinocerebellar atrophies (especially Friedreich’s ataxia).2 They are small, conjugate saccades, ranging from 0.5 to 5.0 degrees in size, which take the eye away from the fixation position and then return it there after a period of about 200 ms. They may be most evident during smooth pursuit, and are easily detected during ophthalmoscopy.
Macrosaccadic oscillations (fig 1F) usually consist of horizontal saccades that occur in bursts, building up and then decreasing in amplitude, with intersaccadic intervals of about 200 ms.4 These oscillations are usually induced by a gaze shift. They are a sign of midline cerebellar disease (affecting the fastigial nucleus), including spinocerebellar degenerations (see video, “Macrosaccadic_oscillations”),24 but have also been reported with pontine lesions.25
Saccadic pulses are brief intrusions that take the eye movement away from the fixation position, with a rapid drift back. They are reported in patients with internuclear ophthalmoplegia.26 There is a continuum between saccadic pulses and saccadic oscillations without an intersaccadic interval (fig 1G). The latter may occur in the horizontal plane, ocular flutter,27 or may consist of saccadic oscillations with horizontal, vertical, and torsional components, opsoclonus (see video, “Opsoclonus”). The frequency of oscillations is usually typically 10 to 15 cycles per second, being higher with smaller size movements. Flutter and opsoclonus are often brought out by eye lid closure or during gaze shifts between far and distant targets.28 Most cases of flutter and opsoclonus conform to four main diagnostic groups: parainfectious brainstem encephalitis (including multiple sclerosis),27 paraneoplastic syndromes, metabolic-toxic states, or idiopathic. Differentiation between these disorders depends on the general neurological findings and laboratory testing.29
This research was supported by USPHS grant EY06717, the Office of Research and Development, Medical Research Service, Department of Veterans Affairs, and the Evenor Armington Fund (to R J Leigh).
By: William C. Head, Criminal Defense Attorney Atlanta GA and ABA Board-Certified DUI Attorney
Don’t Take Field Sobriety Tests!
If you have recently been arrested for driving under the influence (DUI) after failing the field sobriety tests, it may be too late to tell you that these sobriety tests are completely voluntary (that is, you can’t be punished for declining to take them).
But it’s never too late to challenge your results. The officer’s scoring on the field sobriety tests is completely subjective, which means that his or her bias could result in a failing grade. Because of this deception, you should work with an Atlanta DUI attorney who can review your field sobriety evaluation test to determine if it was scored fairly, or if there were other factors (like overweight, orthopedic issues, inner ear problems) that affected your performance.
Challenging the Georgia Field Sobriety Tests
Despite a complete lack of a scientific basis, a police officer can use a number of field sobriety tests, such as reciting the alphabet backwards or touching your nose with your eyes closed, to see if you are impaired.
However, only three tests are approved by the National Highway Traffic Safety Administration (NHTSA): the walk and turn, one leg stand, and horizontal gaze nystagmus. DUI lawyers will use “shorthand” to identify these sobriety tests as WAT, OLT, and HGN. Another rarely given test is called the vertical gaze nystagmus, or VGN.
The walk-and-turn and one-leg stand tests both measure your ability to follow simple instructions as well as to complete a physical task. The theory is that both of these abilities become diminished once a person is under the influence of alcohol. However, other factors could affect how a person performs these tests.
For example, an individual who has a physical problem, is overweight, or is over a certain age (40 or over) may have a hard time successfully completing these tasks. Just being nervous and shaking, due to the stress of your situation, may cause you to be unable to perform them at all. Wearing the wrong shoes or even being nervous can also make getting a passing score more difficult.
The horizontal gaze nystagmus test has a medical origin, but is NOT used by physicians to guess your alcohol level. During the administration of this test, an officer will ask you to follow an object with your eyes while he or she looks for your eyes to jerk (a sign of possible central nervous system issues).
However, a number of other physical and neurological conditions can also cause this involuntary jerking as you look side to side. Doctors do a similar evaluation, in a dark room, when evaluating HEAD TRAUMA. An attorney can work with a medical expert to determine if a condition—other than the consumption of alcohol—is responsible for nystagmus.
How the Federal Government Pushed the Use of Field Sobriety Tests
As drunk driving cases increased, and citizens hired criminal lawyers to fight their DUI-DWI cases across the country, a disturbing trend of victories by DUI defense lawyers became apparent.
Jurors would hear the evidence, and see some made-up sobriety tests being given (like picking up four coins in their sequence of value, from lowest denomination to highest, or tracing a circle with a pencil, or attempting to count backward, or blowing into a hat) and simply not find that this “proof” meant anything.
Acquittals increased as the DUI attorneys became more skilled at fighting driving under the influence charges.
The lack of some UNIFORM method of SCREENING possible drunken drivers at the roadway was apparent to all. No approved methods for screening drinking drivers existed in any state. One officer would make up some tests, and then pass it on to others. Soon, it became a joke to think that these ad hoc exercises could point to sobriety or the LACK thereof.
Marcelline Burns, a Ph.D. candidate in college in California, wrote her thesis on drunk driving, and suggested a NATIONAL need for “standardized” roadside tests that would have SOME correlation to DWI-DUI. Her supervising professor (Dr. Herbert Moskowitz) suggested that she send the paper to NHTSA, a federal agency that oversaw highway safety.
This acronym stands for “National Highway Traffic Safety Administration” and is part of the United States Department of Transportation. His idea was to help her try to get a government contract to STUDY the idea, and formulate some appropriate, standardized tests.
Dr. Burns’ letter to NHTSA pointed out the extreme need for a “battery” of quick and uncomplicated roadside tests to be used by police officers to make better arrest decisions, and to CREATE standardized evidence that could “hold up” in court.
Always looking to find a better way to identify impaired drivers who were violating the law, as opposed to drinking drivers who were in compliance with the law, must have struck a chord with the NHTSA brass because Dr. Burns landed a HUGE government contract.
The Goal: Create Fair, Scientific, and Standardized Sobriety Tests
Dr. Burns’ challenge was to create a few, easy-to-administer, quick roadside tests, which would be FAIR sobriety tests. Her investigation into which were the BEST tests would be overseen and documented by trained observers who had a scientific background.
Next, the voluminous results obtained after screening (and re-screening) hundreds of test subjects, would be studied by her team to find the MOST reliable of the ten original tests investigated. The HOPE was for the final field sobriety tests to be proven to be highly accurate at predicting which drivers were at or above the legal limit for alcohol of 0.10 grams percent (at that time). Then, the team had to narrow down these “tests” to those that could be objectively standardized, controlled and uniformly taught to be given in a fixed, systematic manner to police officers all across America.
Unfortunately, while basic “scientific method” was used in two studies (1977 and 1981), the effort was begun to CREATE the statistical data and “numbers” before any NORMS were first established. This doomed the effort due to flawed methodology.
By this I mean that no INITIAL testing was done on large groups of totally sober individuals, in various AGE groupings, with various health issues (e.g., overweight individuals, those with prior orthopedic injury or surgery, or those taking prescribed pain medications or anti-anxiety medications.)
So, no BASELINE existed to JUDGE how the dosed drinking driver test subject compared to totally sober people 50 and older, or totally sober men and women who were 50 or more pounds overweight.
This oversight and shortcoming would never pass muster with true research scientists who are not driven by creating SOMETHING in order to get paid. Common sense tells us the answer, whether the two women try to stand on one leg with their arms to their sides, or whether they attempt a few gymnastics on a balance beam. The obese woman is heading to jail, drunk or not!
One of the most important items (for your DUI lawyer) to PROVE “unfairness” is the total omission of any advisement that ALL field sobriety tests are OPTIONAL, VOLUNTARY, and have no bearing on your driver’s license. Additionally, no advisement is given that — at the conclusion of your ATTEMPT to perform the evaluations—you will not be allowed to have any “do-overs” for your earlier, failed performances.
The stated GOAL for standardized field sobriety testing was “to make our highways safer” by removing drunk drivers through utilizing better police training on the proper methods of roadside screening of suspected drunk drivers for alcohol impairment through psycho-physical testing. The end result was to print up a lengthy manual that is handed out to police officers in a 20-hour class.
The officers usually learn perhaps 10 to 15 pages of the 200+ page manual, all focused on how to arrest people who have been drinking alcohol.
These manuals (which have now been re-done and altered over a dozen times since 1984) have NEVER been peer-reviewed, or published in a scientific journal.
This vetting should have been done to get feedback about defects and deficiencies in the police instruction, scoring methodology, and the teaching of the TRUE lack of reliability that these evaluations reveal in the limited statistics that were collected and retained.
Thousands of drunk driving arrests, however, have been and ARE currently being made because of these faulty evaluations. Independent researchers have undertaken an analysis, after many convicted citizens cried “foul” on these bogus tests.
The only thing standing between a conviction for DUI and an acquittal is an experienced, well-trained, savvy criminal defense attorney who is a DUI lawyer and a specialist in fighting field sobriety test evidence.
The Achilles Heel of the Standardized Field Sobriety Tests
The biggest and most insurmountable flaw in Dr. Burns’ team’s work is that the sobriety test “battery” was never correlated to any NORM groupings for proving the reliability of the final three field sobriety tests used by Burns and her research team. Moreover, only partial data was retained by the researchers, and (once released) this gave reviewers only partial data for later analysis. The assumption has to be that the unreported numbers were UNFAVORABLE.
These experts have now concluded that non-disclosure of all data makes review of her methodology only partially available, and (therefore) is unconvincing. Other researchers who have tested the three SFSTs found similar “false positive” numbers of 46%, which (as Burns admitted) was “unacceptable.” This is no better than flipping a coin.
True scientists who specialize in statistics, testing, and measurement, and human factors have used words like UNRELIABLE, FRAUD, INCONCLUSIVE, and INCOMPLETE to characterize these tests that have been the basis of millions of DUI arrests.
Cursory training by police officers who erroneously believe that field sobriety test evidence is the best thing since the wheel was invented has led to the false belief that these tests SHOULD be good for evaluating DUI-Drugs, too.
Dozens of federal grants have been awarded to Burns and her cohorts. In today’s dollars, the total grant money is between $4 million and $5 million dollars. No other contractor was “included” because NHTSA had its “resource” for giving the police a tool to BACK UP their questionable DUI-DWI arrests.
THIS is why potential arrestees were never to be told that the evaluations were optional, non-scientific, and would come down to the officer’s best guess. In no way do these roadway tests (eye test, balance test and walk the line test) come close to the 90% or greater reliability of IQ tests, SAT tests, or ACT tests. Reliability means REPEATABLITY, where the same evaluator tests the same subject under the same test conditions, and gets the same result.
Do I Need a DUI Lawyer? Searching for The Best DUI Attorney in GA
Some people foolishly try to self-assess their chances of winning the DUI in GA. The operable word here is “FOOLISHLY.” Just reading TRUE DUI case histories with: (1) BAC levels triple the alcohol legal limit, or (2) with a DUI refusal and failing all three NHTSA field sobriety tests, or (3) another drunk driving case report of a DUI checkpoint with a Intoxilyzer breath test double the legal alcohol limit, from two of our previous criminal trials will dissuade you from thinking that you have no chance to beat a DUI in court.
After being arrested for DUI in GA, some people are so depressed that they dwell on their mistake the night before, and not on beating the criminal charges. Fear of the unknown can be a powerful enemy. Our DUI lawyer partners WELCOME comparing criminal attorney comparisons. For example, our law firm has three different law book authors, which is unique in Georgia and possibly in all of America.
A successful defense record for all Atlanta DUI attorneys in the law firm must include possessing the ability to neutralize field sobriety test evidence and finding ways to eliminate breath alcohol test results, especially where the “number” is in excess of the legal alcohol limit. Plus, know the LAW is critical, and this entails our DUI attorneys being familiar with every prior appellate decision on Georgia DUI laws and especially the Georgia implied consent law.
Drugged driving cases have grown by 100% in the last 15 years. Sleep driving DUI cases, after taking prescribed medications for insomnia or pain management are up by 400%. Plus, a conviction for DUI-drugs has more devastating DUI penalties in Georgia that a DUI-alcohol case, due to more severe loss of driving privileges and other loss of entitlements (e.g., loss of the GA Hope Scholarship due to a “drugs” conviction).
Each DUI attorney in our law office possesses special training on debunking “drug recognition” officers’ training and roadside tests like the “modified Romberg test” and the less-extensive ARIDE protocols require that our criminal defense lawyers know how to challenge a GBI blood alcohol or drugs test. Each of our Atlanta lawyers are an INSTRUCTOR in the three NHTSA standardized field sobriety tests (SFST), which exceeds the training of most police officers making arrests for DUI in Georgia.
The best DUI lawyers in Atlanta, Georgia will offer you a FREE attorney consultation, explain how their criminal defense attorneys review your DUI case facts and implement a game plan for winning. Our three Georgia Super Lawyers aggressively represent clients accused of committing crimes through filing and arguing suppression motions. Limit your search to a lawyer for DUI who has achieved legitimate legal industry excellence attorney ratings, and who possesses a track record of proven drunk driving defense results on knowing how to beat a DUI. If our law firm has the RIGHT criminal defense attorney for you, ask our law office about our DUI attorney payment plans.
Call our DUI attorneys NOW, 24-7, for an initial criminal case review and to obtain FREE legal advice: 404-567-5515, or email our criminal justice lawyers.
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