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Horizontal Gaze Nystagmus

February 13, 2008

Nystagmus is a rhyth­mic, tremor-like movement of the eye. Crudely defined as a pulsation or twitching which occurs with a lateral or horizontal move­ment of the eye, when associated with alcohol it is not a new phenomenon. The effect of alcohol upon eye motions having been observed in animals as early as 1826. 1897 saw the first published report not­ing the occur­rence of nys­tagmus in hu­man beings following the consumption of etha­nol.[i] In 1911, re­searchers noted that alcohol in­duced nys­tag­mus under­went a change as the head was moved from the left lateral to right lateral posi­tion. Called Positional Alcohol Nystagmus or PAN, detailed studies in the late fifties by Aschan[ii] documented a downward motion during the ab­sorption phase called (PAN I), a period with no posi­tional nystag­mus lasting approximately 90 minutes and a period of movement toward the uppermost ear that coin­cided with elimina­tion of alcohol from the system (PAN II).

While positional alcohol nystagmus is of concern to those entrusted with attempting to figure out the cause of automo­bile and aircraft acci­dents,[iii] it is not viewed as a par­ticu­larly reli­able indicium of in­toxica­tion. For that we turn to Hori­zon­tal Gaze Nystag­mus or HGN.

HGN is a form of gaze nystag­mus or pulsation that is in­duced by lateral devia­tion of the eye. By lat­eral de­vi­a­tion we mean the hor­i­zontal motion that is produced when the eye is drawn to the left or right by the ex­amin­er. It is not pres­ent when the eye is look­ing straight. The point where this rhythmic pulsation first oc­curs is known as the angle of on­set, the determination of which is criti­cal when attempting to use HGN for determining in­toxi­cation.

Also dis­cussed with HGN is the concept of smooth pur­suit or the ability of the eye to track a moving object smoothly It represents an impairment of the neural mecha­nisms that con­trol the movement of the eye and can be brought on by the ingestion of alcohol.

Of paramount importance in the inability of the eye to maintain a consis­tent lateral gaze, or HGN, is a docu­mented correlation between a de­crease in the degree to which the eye can gaze to the side, and an increase of blood alcohol content (BAC). First not­ed by Lehti in 1976,[iv] Tharp, et. al., de­vel­oped the fol­lowing equa­tion to de­scribe the degree to which lat­eral gaze was af­fect­ed:

O ' 51 G 100 (BAC as % w/v)

Solving for the angle of onset [O] or the point where pulsation is first observed, the following simplification has been de­vel­oped for use in the field:

BAC ' 50 G Angle of onset.

In theory, this formula is fairly easy to employ. The administering officer con­structs a 90 de­gree angle by first drawing an imaginary line through the mid­line of the skull. This line repre­sen­ts zero de­grees. A second imaginary line perpen­dicular to the first and drawn through the ears becomes 90 de­grees. Thereafter, the officer, by smoothly moving a target such as a pen or penlight watches for the onset of pul­sation. The point at which this action is first noted is the "angle of onset." This means that if the onset angle was 40 de­grees, then the BAC would be expected to be approx­i­mate­ly .10% (50 G 40). Likewise, with an on­set an­gle of 35 de­grees one would expect to find a BAC of .15% (50 G 35).

In a study conducted by Goding and Dobie,[v] 37 patients in an emergency room were tested using the above for­mula. Of 20 patients with a BAC in ex­cess of .20% w/v, 17, or 85%, had an an­gle of onset of less than 30 degrees and all 20 showed onset at 40 degrees or less. The measured BAC of six patients was between .10% and .20% and five of the six had an angle of onset of 40 degrees or less. In one patient with a BAC of .155%, onset occurred at 45% suggesting a BAC of .05%.

In the eleven patients that re­mained, the results were not as good. Four patients with a BAC of less than .10% had an angle of onset of less than 40 degrees, thus falsely indicating intox­ication. These false positive were found as a result of drugs such as di­phenhydramine, phenytoin and me­peri­dine.

When the authors conducted a simi­lar examination using experienced members of the Seattle police depart­ment, BAC esti­mating errors were had in approximately 10% of the cases, of which 86.86% resulted in overestima­tion, in one instance as great as .09%.

While Goding and Dobie achieved results greater than the 78% predicted by Burns & Moskowitz in their 1981 study,[vi] it must be recognized that this was a comparatively small sample and that the an­gle of on­set was mea­sured us­ing a nys­tag­mus pro­tractor, whereas in actual prac­tice nys­tagmus is crudely esti­mated us­ing crutches such as the disap­pear­ance of the white of the eye. In­deed, even NHTSA recog­nizes the need for accura­cy in adminis­tration, not­ing that "nys­tagmus an­gle of onset is an ex­cellent tool for pre­dicting the BAC when it is measured with suffi­cient pre­cision."[vii]

Moreover, not all researchers agree on the existence of a relationship be­tween the angle of onset and BAC. Norris,[viii] for instance, rejected the exis­tence of virtually any relationship be­tween onset and BAC. Others, most notably Aschan, the grandfa­ther of Nys­tagmus research, described a 40 degree angle of onset at a BAC of .06% and found nystagmus to persist for more than five hours after the disappearance of all alcohol from the body.[ix] Al­so, there exists a lively debate as to occur­rence of "normal nystagmus." While NHTSA places this figure at 4.4%, Toglia states that nystag­mus at 40 de­grees and great­er exists in 50-60% of the sober popula­tion.[x] Even the hour of administra­tion may have a role to play. Tharp, et. al., in a 1981 NHTSA study[xi] reported that "the ef­fects of fatigue or cir­ca­dian rhythms on gaze nystagmus could be significant," observing that "the alcohol dose de­creased the angle of on­set by an addi­tional five degrees after mid­night." Finally, de­tec­tion of HGN is com­pli­cat­ed by the pres­ence of end point nys­tag­mus or pseudonystag­mus. This phenom­enon, which occurs nor­mal­ly in many individ­uals, disap­pears when the gaze is shifted centrally, or toward the nose a few de­grees. Pseudonystag­mus, there­fore, strongly resembles HGN and has been described in the literature as dif­ficult to deter­mine from true nystag­mus.[xii]

While several New York police agen­cies, most notably the New York State Police, routinely employ HGN for detecting and measur­ing intox­ication, a close examination of the tech­nique as em­ployed raises grave concerns. For instance, NHTSA instructs the of­ficer to observe the subject and take note of "the first sign of jerking." HGN, how­ever, is far more than "jerking." An of­ficer looking merely for "jerking" may record rotary or PAN, although both are undesired side affects. Whereas NHTSA adminis­tered placebos to those with natural nystagmus or who were taking prescription drugs known to pro­duce such results, in practice officers do not take an adequate history prior to administration of the test. Troublesome is that given the "jerking" definition that is taught, a history should include all alcohol consumption within the last 24 hours. Given the circum­stance in which the test is administered, it does not seem probable that a forth­right history can be obtained. Contact lenses also create problems. Whereas NHTSA now recommends that they be re­moved,[xiii] officers frequently fail to ask if they are being worn and of course re­moval under the circumstances creates difficulties that are perhaps insur­mountable.

Perhaps the greatest impediment to the use of HGN is its unquestioned lack of specificity. As recently recog­nized by the Supreme Court of Kansas in State v Witte, (1992) 836 P.2d 1110: "Nystag­mus can be caused by problems in an individual's inner ear * * *. Physio­logi­cal problems such as certain kinds of diseas­es may also result in gaze nystag­mus. Influen­za, streptococcus infec­tions, ver­tigo, measles, syphilis, arterio­sclerosis, muscu­lar dystrophy, multiple sclerosis, Korsakoff's Syndrome, brain hemor­rhage, epilepsy, and other psycho­genic disorders all have been shown to cause nystagmus. Furthermore, condi­tions such as hypertension, motion sick­ness, sunstroke, eyestrain, eye muscle fatigue, glaucoma, and changes in atmo­spheric pressure may result in gaze nys­tagmus. The consumption of common substances such as caffeine, nicotine, or aspirin also lead to nystagmus almost identical to that caused by alcohol con­sumption."

While cases regulating HGN run the gamut, in New York, the test has been rejected on foundational grounds. In People v Erickson, (1989, 3rd Dept) 156 AD2d 760, 549 NYS2d 182, the Court found ad­mis­sion to be error, albeit harm­less. A similar out­come was reached in People v Torrey, (1988, 3rd Dept) 144 AD2d 865; 534 NYS2d 807. In Torrey, the Third De­part­ment, cit­ing the Frye stan­dard, found the proof in­suf­fi­cient to warrant admis­sion, although such ad­mis­sion was ulti­mately held to con­stitut­e harm­less er­ror.

When confronted with HGN, ques­tion the officer as to his or her training. If the officer will admit that the NHTSA publica­tions are authoritative, explore with particularity the degree to which he or she followed its procedures. If the officer ac­knowledges the danger presented by contact lenses or organic conditions such as seizure disorders, see if an adequate history was taken. If it appears that HGN will be an issue at trial, explore the possibility of retaining an ophthalmologist or an optometrist to testify as to the nonspecificity of the tech­nique. While we will leave it to others to characterize the officer's tech­nique as "eye-balling," it is help­ful to distinguish the officer's examination from the sophisticated tech­niques medi­cally employed for nys­tagmus mea­sure­ment.

[i].Joffroy A., Serveaux R., NMensuration de la toxicité vraie de l'alcool éthylique: symptômes de l'intoxication aigu et de l'intoxication chronique par l'alcool éthylique. Arch. Méd Exp 1897;9:681-707.

[ii].Aschan G., "Different Types of Alcohol Nystagmus," Acta Otolaryngol, 1958:140:69-78.

[iii].Gibbons, Harry L., Alcohol, "Aviation, and Safety Revisited: A Historical Review and a Suggestion," Aviation, Space and Environ­mental Medicine, July, 1988, pp 657- 660.

[iv].Lehti, H., "The Effects of Blood Alcohol on the Onset of Gaze Nystagmus," Blutalkohol, 13:411-414, 1976.

[v].Goding, G. S., Dobie, R. A., "Gaze Nystagmus and Blood Alco­hol," The Laryngscope 96:July 1986, pp. 713-717.

[vi].Burns, M., and Moskowitz H., "Psychophysical Tests for DWI Arrest," National Highway Traffic Safety Administration Contract No. DOT-HS-5-01242 (1977).

[vii].|Emphasis supplied herein\

[viii].Norris, "The Correlation of Angle of Onset of Nystagmus with Blood Alcohol Level: Report of a Field Trial." 25 Journal of Forensic Science 476 (1986).

[ix].Aschen, Bergstedt, Goldberg, & Laurell, "Positional Nystagmus in Man During and After Alcohol Intoxication," 17 Q.J. of Studies on Alcohol 381, Sept., 1956.

[x].Toglia, Electronystgmography: Technical Aspects and Atlas, (1976).

[xi].Tharp, Burns and Moskowitz, "Development and Field Tests of Psychophysical Tests for DWI Arrest," DOT-HS-805-864 (1981).

[xii].Walsh, F. B., Hoyt, W. F., Clinical Neuro-Ophthalmology, 3rd ed., vol. 1, p. 283.

[xiii].DOT-HS-806-512 (1984).

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