Seattle, Washington, Field Sobriety Test Defense LawyerHave you ever wondered if you are required to take a "field sobriety test" when a police officer pulls you over for suspicion of drunk driving? I am DUI defense attorney Peter J. Peaquin. When you call my law firm, I will tell you that you are absolutely under no legal obligation to take a "field sobriety test." Although your refusal to perform "field sobriety tests" may be admissible at trial, the officer's comments regarding your performance on what in reality are "field dexterity tests" may be more damaging. I provide a free consultation to discuss your HGN test resultsAll major credit cards accepted and payment plans may be availableThe horizontal gaze nystagnus (HGN) test is one of the field sobriety tests (or FSTs) used by police on the city streets and highways of Washington State. The HGN test was not developed to determine a person's level of impairment and it is not an accurate indication of a person's level of intoxication. Even the government's own studies, conducted on behalf of the National Highway Traffic Safety Administration, show that the PROPERLY administered entire field test battery was less than an 80 percent rate of accurate in predicting a breath test level greater than .10. The HGN test measures impairment in the vestibular system, the system that governs the ability of the human body to maintain balance and orientation. The HGN test DOES NOT measure any impairment in the ability of a person to operate a motor vehicle. I invite you to read more specific information about the HGN test by reading the following information. If you have been charged with DUI based on your eye movement, you may have a very valid defense. Contact me right away to start aggressively protecting your rights. Cli Understanding the Physiology Behind the Horizontal Gaze Nystagmus Test. “What is nystagmus? Do I have it? Do I want it? Is it contagious?”Nystagmus is the "oscillation of the eyeballs, either pendular or jerky". Stedman's Medical Dictionary 971 (5th ed. 1982). This involuntary movement results from the body's attempt to maintain orientation and balance. HGN is the inability of the eyes to maintain visual fixation as they turn from side to side or move from center focus to the point of maximum deviation at the side. State v. Cissne, 72 Wn.App. 677 (1994). The ability of the human body to maintain balance and orientation is governed by the vestibular system. The vestibular system is composed of a pair of five sense organs: three semicircular canals, the utricle and saccule, located on the right and left sides of the head. The three semicircular canals (posterior, anterior, horizontal) are at right angles to each other (orthogonal) and detect rotation. The otolithic organs sense motion according to their orientation. The utricle is mainly horizontal and largely detects lateral accelerations. The saccule is vertical, and detects acceleration up and down. The information detected by these organs is sent by nerves to the centers of the brain that interprets this input, control eye movement and the muscular system that coordinate the ability to stand upright. Signals from the semicircular canals are sent as directly as possible to the eye muscles to maintain clear images on the retina during head movement. This direct pathway of three neurons is called the “Three Neuron Arc.” The ability of the human body to coordinate these movements is known as the Vestibulo-ocular reflex. Impairment of this reflex by disease or injury can inhibit the ability of the brain to detect head movement, and therefore, coordinate eye movements. It should be of interest to those charged with a DUI that diseases of the vestibular system can induce vertigo, lack of balance, and are often accompanied by nausea. The most common ones are Vestibular neuritis, a related condition called Labyrinthitis, and Benign Paroxysmal Positional Vertigo (BPPV). The vestibular system can be affected by tumors on the cochleo-vestibular nerve, tissue damage in the brain stem or in cortical regions where vestibular signals are interpreted and cerebellar atrophy. Vertigo can also be caused by consumption of alcohol. NystagmusWhile nystagmus can be defined as a rapid “oscillation of the eyeballs, either pendular or jerky” the defining characteristic of nystagmus is that the movement of the eye is “involuntary.” Nystagmus can be induced by rotating a person with their eyes closed. Upon stopping the rotation and opening their eyes, the jerking of the eyes from side to side should be visible. (Rotary-induced nystagmus) Optokinetic nystagmus (also called opticokinetic nystagmus) occurs when an image moves across the retina. It is a rhythmic to and fro movement of the eyes with a fast and slow phase that is identical to the nystagmus evoked by stimulation of hair cells in the semicircular canals. For example, as the visual scene moves from right to left across the retina, both eyes are driven slowly to the left to maintain the image of the visual target on the fovea of the retina. When the eyes reach the limit of their left lateral gaze, they shift rapidly back to the right to capture another target for foveation and, because the target is moving to the left, the slow movement to the left begins again. This cycle repeats rhythmically. The occurrence of optokinetic nystagmus confounds the observation of vestibular-evoked nystagmus at the beginning of a rotation. Optokinetic nystagmus is a normal response and can easily be elicited by having an individual observe a horizontally moving pattern of vertical black and white stripes. Medical College of Georgia, Essentials of Human Physiology, Chapter 7, Brain Function, Balance and Equilibrium S. D. Stoney, Jr. Ph.D. http://www.lib.mcg.edu/edu/eshuphysio/program/section8/8ch7/s8ch7_24.htm The normal manifestation of nystagmus not only varies greatly between individuals, but it also varies greatly within the same individual at different times. The implications of this fact in the realm of the forensic application of the horizontal gaze nystagmus test should not be overlooked. The occurrence of nystagmus can be described as:
Horizontal nystagmus is also classified into three degrees: First degree nystagmus is present only on lateral gaze, and has the fast phase in the direction of gaze; Second degree nystagmus is present in the primary (neutral) position of gaze; Third degree nystagmus is present in the same direction in all gaze positions Such distinctions help to identify the anatomical source of the nystagmus. First degree nystagmus usually originates in the brainstem or cerebellum, while second and third degree nystagmus are usually vestibular in origin. Nystagmus can be “caused” by disease. Nystagmus is present as a pathological sign in:
Acquired nystagmus may be present with; visual loss associated with dense cataract, trauma or cone dystrophy; Central nervous system disorders such as thalamic hemorrhage, tumor, stroke, trauma, multiple sclerosis, Toxic or metabolic abnormalities including alcohol intoxication, lithium, barbituates, phenytoin(Dilantin), salicylates, benzodiazepines, phencyclidine, other anticonvulsants or sedatives, Wernicke's encephalopathy, thiamine deficiency. Development of DWI Psychophysical Tests For DWI Arrest.The current incarnation of Standardized Field Sobriety Tests grew out of the work of the Southern California Research Institute performed under contract to the United States Department of Transportation, National Highway Traffic Safety Administration. Their final report issued in June, 1977 described alcohol gaze nystagmus, Alcohol Gaze Nystagmus (AGN)The jerking movement of the eye, which is known as Alcohol Gaze Nystagmus, occurs upon lateral gaze when BAC exceeds a critical level (≈.06%). The eye jerks in the direction of gaze, independent of head position. Person is asked to cover one eye and follow movement of a small light or object with other eye without changing head position. Light is moved slowly to points requiring 30° and 40° lateral deviation of the gaze. Test is then repeated with the other eye. Eye is observed for jerking movement. DOT HS-802 424 Following the initial report, The Southern California Research Institute secured another grant to “complete the laboratory development and validation of the sobriety test battery identified by Burns and Moskowitz (1977).” Development And Field Test Of Psychophysical Tests For Dwi Arrest, V. Tharp, M. Burns, H. Moskowitz, DOT HS-805 864. As part of this contract, Tharp, Burns and Moskowitz performed a literature review of the variables affecting the “three test battery” first identified in the 1977 contract. Portions of the “Appendix A” relate specifically to horizontal gaze nystagmus (HGN). APPENDIX AAlcohol and NystagmusNystagmus refers to a jerking of the eyes which may be pendular (equal on both sides) or asymmetric with a slow and fast phase (Toglia, 1976). Alcohol appears to influence a number of different kinds of nystagmus, including: positional Nystagmus (Aschan, 1958; Goldberg, 1963), post-rotational nystagmus (Schroder, 1971b), caloric nstagmus (Schroder, 1971b), optokinetic nystagmus (Schroder, 1971a), gaze nystagmus (Aschan, 1958; Lehto, 1976). If all of these forms of nystagmus are considered, then the literature on alcohol and nystagmus is quite large and somewhat contradictory. However, by studying the mechanisms producing nystagmus, the literature can easily be sorted. Essentially, alcohol can influence nystagmus in two ways: (1) mechanically by acting on the vestibular system, and (2) neurologically. Vestibular Mechanisms (See Howard and Templeton, 1966)In man, three semicircular canals, joined at right angles, are located in each inner ear. The canals are filled with fluid called endolymph. A swelling or ampulla is located in each canal and contains the sensory transducer of the canal. Essentially, the cilia of a number of sensory cells project into a common gelatinous mass, the cupula. This cupula is hinged at one end, so that it can swing from side to side with the ampulla. In the upright position, the cupula forms an effective seal, preventing the leakage of endolymph past that point. The semicircular canals respond to angular acceleration, such as in a head movement, which causes the endolymph to lag behind the head movement (i.e., the fluid moves) and deflects the cupula. Deflection of the cupula discharges the sensory cells and provides the sensation of movement. With constant angular acceleration, the system provides accurate information for the first ten seconds or so and then underestimates the amount of acceleration. If the person is then held at a constant velocity, then the cupula catches up to the skull movement (i.e., it returns to normal position) and the sensation is one of slowing down and eventually (in about 20 seconds) of stopping. If the person is stopped, then he or she will sense a sudden acceleration in the opposite direction because the head is now slower than the endolymph, which causes the cupula to deflect in the opposite direction. If the person remains stopped, then the cupula returns to its level position giving a sensation of slowing down and stopping. Since the three semicircular canals in each ear are at right angles, we can sense angular acceleration in any direction. When visual information conflicts with the sensation of motion, one feels dizzy and may feel sick. However, the mere sensation of movement may produce illness in some individuals. The vestibular system interacts with the visual system by producing alternating fast and slow eye movements (i.e., nystagmus) in addition to the sensation of movement. Nystagmus is produced because the eye is lags behind the angular acceleration, so a “brain center” makes periodic adjustments in order to maintain adequate foveal fixation. For example, one can move one’s head back and forth and still maintain fixation. Unfortunately, angular acceleration is not the only stimulus which will cause cupular deflection. The cupula and endolymph both have the same specific gravity. A very slight change in the specific gravity of either the fluid or the cupula may result in a cupular deflection, because the system becomes sensitive to gravity with certain head positions. Money and Miles (1975) claim that a change in the specific gravity of 3 parts in 100,000 will make the system sensitive to gravity. Alcohol and some other drugs can alter the balance in specific gravity (Money and Miles, 1974; 1975). The base of the cupula has a rich blood supply. Foreign substances in the blood will diffuse rapidly into the cupula because of its proximity to the blood and alter the specific gravity of the cupula with respect to the endolymph. The direction of the nystagmus (i.e., the fast phase) will depend upon whether the drug makes the specific gravity of the cupula greater or less than that of the endolymph. For example, within one hour after consuming alcohol a positional alcohol nystagmus (PAN). will occur. That is, if from supine position one rolls one’s head to the side (i.e., so that the cupula is subject to gravity), a nystagmus, called PAN I, occurs in which the fast eye movements are down (e.g., Aschan and Bergsted, 1975). Approximately four hours after drinking, the nystagmus stops. This is probably because sufficient alcohol has diffused into the endolymph so that its specific gravity equals that of the cupula. Finally, as alcohol is eliminated from the bloodstream, the endolymph ends up with a greater concentration of alcohol than the cupula. At this point, a positional nystagmus occurs in which the fast eye movements are up (PAN II). PAN II may persist up to 20 hours after consuming alcohol—long after alcohol has been eliminated from bloodstream (Hill, Collins, and Schroeder, 1973). In fact, under conditions of increased gravity, PAN II has been found up to 40 hours after drinking alcohol (Oosterveld, 1970). The change in specific gravity also explains why the presence of congeners in alcohol can increase the amount of positional nystagmus (Murphere, Price, Greenberg, 1966; Ryback and Dowd, 1970). Excellent reviews of the PAN phenomenon are contained in Aschan, Bergsted, Goldberg, and Laurell (1956); Fregly, Bergsted and Graybiel (1967); Hill, Collins, and Schroeder (1973); Aschan and Bergsted, (1975); Aschan, (1958); and Goldberg 1963. PAN I intensity provides a rather good indication of the peak BAC (Goldberg, 1963), but not of the duration of the intoxication. PAN II intensity has been correlated with hangover effects (Goldberg, 1963). 2. Neural MechanismsAlcohol affects nystagmus in an indirect way—by inhibiting the neural mechanisms involved in maintaining visual fixation. In some instances, visual fixation acts to inhibit nystagmus. Thus, if a vestibular signal tells one that rotation is occurring while visual information conflicts, then the visual information usually wins but often at the expense of producing nausea. Irrigating the ears with warm or cold water starts the endolymph fluid moving and produces a nystagmus called caloric nystagmus (e.g., Schroeder, 1971a). Visual fixation will inhibit this nystagmus, but not after taking alcohol (Schroeder 1971a). Similarily, rotational nystagmus or post-rotational nystagmus can also be suppressed by visual fixation. But fixation again is ineffective after taking alcohol (Schroeder, 1971b). Both levels of arousal, suggesting the alcohol suppression may also be due to the sedative effect of the drug (Collins, 1963; 1973). In all of the above examples, nystagmus is produced by vestibular activation and alcohol acts to suppress that nystagmus. However, alcohol reduces nystagmus that is not produced by vestibular activation. Optokinetic nystagmus, for example, is produced by watching a rotating drum covered with alternating black and white vertical strips (Mizoi, Hishida, and Maeba, 1969). It consists of a slow component in the direction of the moving object (or strips) and a quick phase in the opposite direction. Mizoi, Hishida, and Maeba (1969) describe four phases of optokinetic nystagmus: First, the slow eye movements keep up with the movement of the object. Second, the slow phase eye movements accelerate, but cannot keep up with the stimulus. Third, the slow phase attains its maximum speed. An average person can typically follow a moving object up to 30 degrees per second. Finally, the eye movement fails. Alcohol impairs optokinetic nystagmus by reducing the maximum speed that can be obtained (Mizoi et al., 1969). The slow eye movements mentioned in connection with optokinetic nystagmus are called “smooth pursuit” movements (Rashbass, 1961; Robinson, 1968). This system for moving the eyes (1) requires a moving stimulus; (2) is virtually autonomic; and (3) is concerned primarily with matching the speed of the eye with the speed of the target (Robinson, 1968). These movements appear to function in providing a stable image on the retina (Rashbass, 1961). Smooth movements do nothing to correct for the position of the target, which is the function of the much faster “saccadic” eye movement system (Rashbass, 1961; Robinson, 1968). The smooth pursuit system appears to be particularly vulnerable to the effects of alcohol (Wilkinson, Kime, and Purnell, 1974). This system normally can track movement at up to 30 degrees per second. Alcohol, however, reduces the maximal tracking speed and, in sufficient concentration, may eliminate smooth pursuit movements entirely. When the BAC is high enough, only the saccadic system (which adjusts the eye for target position when the position difference is above some threshold) remains. Thus, at a sufficiently high BAC, one can only follow a moving object with a series of saccadic jerks. 3. Gaze NystagmusRashbass (1959) claims that the inability to maintain visual fixation is responsible for gaze nystagmus, a jerking movement of the eyes when they are deviated laterally. He argues that only the smooth pursuit system is involved in bringing the eye to a single spot. When the eyes are deviated to the side, slow drifting movements will occur toward the center depending upon the amount of lateral deviation and the ability of the smooth pursuit system to counteract these drifts. When the smooth pursuit system is inhibited by drugs such as alcohol or barbiturates, the slow drifts become large enough that saccadic jerks are required to maintain the lateral gaze. Gaze nystagmus can be seen in 50-60% of all individuals if their eyes are deviated to the extremes, but it is considered to be pathological when it occurs at less extreme (i.e., 40 degrees) deviations (Toglia, 1976). Gaze nystagmus occurs with some types of brain damage (Baloh, Konrad, and Honruba, 1975), but it provides little localizing value in detecting the brain damage except to direct one’s attention away from the peripheral labyrinths of the vestibular system. The data of Baloh et al (1975) does support Rashbass’ theory in that pathological gaze nystagmus correlates with fixation instability. Five of their six patients with fixation instability also showed pathological gaze nystagmus. Gaze nystagmus occurs under several different drugs, including alcohol (i.e., Aschan, 1958), barbiturates (e.g., Bender, O’Brien, 1946), antihistamines (Aschan, Bergstedt, and Goldberg, 1958) and phencyclidine (Linden, Lovejoy, and Costello, 1975). A number of other drugs may also produce gaze nystagmus, but most of the evidence is contained in clinical case reports. Although some articles mention the occurrence of alcohol gaze nystagmus, few detail which parameters are important. Lehti (1976) indicated that the angle of onset from the midpoint of the visual field decreases as a function of increasing BAC. His data suggest that at a BAC of 0.10%, gaze nystagmus will occur at about 51 degrees and, at a BAC of 0.20%, gaze nystagmus will occur at about 29 degrees. The correlation between the angle of onset and the BAC was - .788 for 56 individuals. Most other studies in which gaze nystagmus has been measured involve a cutoff point of 30–40 degrees. Use of a cutoff may explain some of their conclusions. For example, Aschan (1958) used a cutoff of 40 degrees and reported that gaze nystagmus had a distinct threshold BAC of approximately 0.06%. Umeda and Sakata (1978) used a cutoff of 30 degrees and concluded that it was one of the least sensitive eye measures of alcohol intoxication. These conclusions are not at all surprising in view of the data that gaze nystagmus will occur at approximately 41 degrees at a BAC of 0.10%. Aschan (1958) has distinguished between a “fine” gaze nystagmus and a “course” gaze nystagmus. The latter tends to be a slow, large amplitude movement of about 10 degrees. Fine nystagmus tends to be a much smaller amplitude of about 4 degrees. We would expect that the difference in amplitude would only occur at a sufficiently high BAC for saccadic eye movement (i.e., in addition to smooth movements) to be impaired (Wilkinson et al, 1974). When the saccadic system is impaired, a larger drift off target may be required for saccadic correction. Aschan (1958) also reports that gaze nystagmus is more evident with monocular fixation than with binocular fixation. He reported that subjects showing monocular gaze nystagmus at 20 degrees would not show binocular gaze nystagmus until 40 degrees. Toglia (1976) reports that gaze nystagmus tends to be greater in the left eye upon gazing to the left and in the right eye upon gazing to the right. These two phenomena may be the same. Horizontal Gaze Nystagmus PSEUDO-SCIENCEIn the process of synthesizing numerous sources concerning HGN and the development of “Standardized Field Sobriety Tests”, several points come into focus (please excuse the pun). The first concerns the scientific questions regarding what conclusions can fairly be drawn from an “observation” of nystagmus in an individual at the roadside. The second concerns the forensic use of this phenomenon. Although numerous types and cause of nystagmus have been documented, the inability of the officer to distinguish causation of a particular individual’s nystagmus may not only subject a motorist to arrest, but if a court allows the testimony to be offered as evidence of “impairment,” the deprivation of liberty. It is distressing to recognize that the contractors in the development and promulgating of the HGN as a “sobriety field test” appear to have come to the task, not as neutral detached scientists, but as “soldiers on the front line in the battle against the carnage on the highways.” Review of the introduction to the Burns and Moskowitz (1977) report reveal their bias. The studies conducted as a part of the DOT contracts appear to rely solely on literature review, devoid of input from the relevant scientific community. Neuro-ophthalmology and neuro-otology are the disciplines concerned with the physiology, diagnosis and management of diseases involving the visual pathways, the control of eye movements, and vestibular circuits in the cranial nerves, brain stem, cerebellum, and cerebral hemispheres. Recognizing the existence of the phenomenon of nystagmus must be distinguished from the utilization of the phenomenon of nystagmus. The acceptance of the proposition that an individual who has consumed a sufficient amount of alcohol to be “impaired in his ability to operate a motor vehicle” will exhibit horizontal gaze nystagmus DOES NOT establish that an individual who exhibits nystagmus is “impaired in his ability to operate a motor vehicle.” Burns and Moskowitz (1977) repeatedly cite Gunnar Aschan and his article “Different Types of Alcohol Nystagmus” Acta-Oto-Laryngologica (1957). However, it is curious to note that they failed to heed many of his findings that have particular relevance within the context of arrest and prosecution of the “drinking driver.” Of particular note concerns the “threshold value” for “alcohol nystagmus” of as low as BAC 0.03.[1] The interpretation of the variability in “angle of onset” also presents a serious question presented that remained unaddressed by Burns et al. Aschan documented onset at 30 degrees with BAC levels as low as 0.48.[2] Aschan also noted the interaction of antihistamine in producing a nystagmus effect. In reviewing the original development of SFSTs, it is interesting to note that officers utilized a protractor to assist in measuring angles of onset, while today officers just “guesstimate.” It is easy to just chuckle at the way that this “parlor trick” can be used to demonstrate that a friend has consumed a large amount of your alcohol, but we must not forget our “righteous indignation” when the State is allowed to argue to the jury, the fallacy that “Impairment in vestibular system equates to impairment in the ability to operate a motor vehicle.” Horizontal Gaze Nystagmus CaselawAlthough the body of Washington caselaw regarding horizontal gaze nystagmus (HGN) is limited, recent events lead many DUI Defense practioners to believe that litigation concerning the admittance of evidence the administration of a HGN test and what testimony may be elicited from a witness concerning the interpretation of the results of such testing will be the next significant battle to be fought. In State v. Baity, 140 Wn.2d 1 (1999), the Washington Supreme Court began its analysis by stating the issue before the Court. We are asked in this case to determine if a drug recognition protocol, used by trained drug recognition officers to determine if a suspect's driving is impaired by a drug other than alcohol, meets the requirements of Frye v. United States, [citation omitted], for novel scientific evidence. We hold that the protocol meets the mandate of Frye. An officer may testify concerning such drug impairment, subject to the limitations set forth in this opinion, upon meeting the requirements of ER 702 and 703 for the admission of expert opinion testimony. [Emphasis added] The Court described not only the specific additional training that a DRE officer receives, but also focused on the proficiency that the DRE officer must demonstrate as a part of the initial certification, the continued training and the bi-annual recertification requirements. These points are worthy of mention in a “non-DRE” case where the patrol officer has not undertaken the same level of training, demonstrated that certain proficiency, documented recorded ongoing ability and maintains current training. The Court briefly reviewed national caselaw concerning the admissibility of HGN testimony: After careful review of these alternative positions, we agree the underlying scientific basis for HGN testing-an intoxicated person will exhibit nystagmus--is "undisputed, even by those cases and authorities holding the test inadmissible without scientific proof in each case.(holding that a person will show a higher degree of nystagmus at higher levels of intoxication). Even the district court agreed with this proposition, stating: The evidence presented in this hearing establish [sic] that the following propositions have gained general acceptance in the relevant scientific community: (1) the HGN occurs in conjunction with alcohol consumption, (2) that the onset of HGN and its distinction are strongly correlated to breath alcohol levels, . . . (4) law enforcement officers can be trained to observe these phenomena and administer the test[.] Baity at 12. The Court gave short shrift to the Defense concerns regarding the factors that make HGN testing unreliable. In dismissing concerns regarding “false positives and other physiological causes”[3] the Court clung to the perceived basis for the test—“intoxicated people exhibit nystagmus.” The Court appears to abandon the traditional “gate keeper” role and relies upon the near super-human abilities of the DUI Defense attorney to cut through “the smoke and mirrors” to lay bare the test inadequacies logic by means of cross-examination. After all, it goes “to the weight of the evidence, rather than its admissibility.”[4] It is incredibly perplexing that the Baity Court reviewed the same out-of-state cases considered by the Court of Appeals in State v. Cissne, 72 Wn.App.677, 680, review denied, 124 Wn.2d 1006 (1994), where the Court of Appeals stated, We hold that the Frye standard applies to the admission of evidence based upon HGN testing, unless, on remand, the State is able to prove that it rests on scientific principles and uses techniques which are not “novel” and are readily understandable by ordinary. We decline the State’s invitation to follow those few jurisdictions that have concluded that HGN testing meets the Frye standard. The trial court must evaluate, weigh and consider the conflicting evidence before determining whether the test is novel, and if it is novel, whether it is a reliable as an indicator of the probability of impairment or of a specific blood alcohol level. The parties have not brought any of this evidence to the attention of this court or the trial court. Cissne, at 686-687. The Baity court found the DRE protocol and the chart used to classify the behavior patterns associated with seven categories of drugs have scientific elements meriting evaluation under Frye. Baity appeared to limit the officer’s testimony to cases where all 12 steps of the DRE protocol had been undertaken. The language of the decision appears to limit who can testify, “the DRE. officer, properly certified” and what the witness can say, “An officer may not testify in a fashion that casts an aura of scientific certainty to testimony and the officer may not predict the specific level of drugs present in the suspect.” I invite you to learn more about DUI defense through my DUI Practice Center contact me right away if you have been charged with DUI after taking an HGN test. I can help you mount an aggressive defense to fight for the best possible results for your charges. [1] Aschan, “Different Types of Alcohol Nystagmus” Acta-Oto-Laryngologica (1957), page 71 [2] page 72 [3] Baity, at 13-14 [4]Baity, at 14 |
Horizontal Gaze Nystagmus (HGN Field Sobriety Test)
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