Pursuit Defect Nystagmus Pursuit Paretic Nystagmus
and smooth pursuit systems after cerebral hemidecortication. Brain 102:387-403, 1979 5 . Z e e DS, Friendlich AR, Robinson DA: The mechanism of downbeat nystagmus. Arch Neurol 30:227-237, 197‘1
James A. Sharpe, M D
Left Vestibular Involvement Primary-position horizontal jerk nystagmus with linear slow phases is typically caused by vestibular imbalance. Primary-position vertical jerk nystagmus is caused by vertical imbalance in the smooth pursuit system [ 5 ] , be it downbeating or upbeating [2]. The nystagmus beats in the direction of impaired pursuit. The report by Drs Abel, Daroff, and Dell’Osso [ 11 described primary-position horizontal jerk nystagmus in a patient with a posterior fossa tumor. The nystagmus had linear slow phases and exhibited the following features that distinguished it from vestibular nystagmus [ 51: ( 1) failure of the nystagmus slow-phase velocity to increase in darkness; (2) unidirectional impairment of pursuit in the direction of the fast phase; and (3) bidirectional preservation of the vestibuloocular reflex. The authors commented that such nystagmus does not accompany the pursuit paresis occurring ipsilateral to unilateral cerebral hemispheric lesions. They speculated that cerebral disease does not cause nystagmus, either because the brainstem and cerebellum are intact, o r because cerebral damage causes paresis of pursuit, not total paralysis. I wish to point out that unilateral cerebral damage can cause primary-position horizontal jerk nystagmus. In our laboratory, pursuit paretic nystagmus was identified in each of 5 patients studied eight to twelve years after cerebral hemidecortication [4]. Clinical and radiological examination indicated intact cerebellar and brainstem function. The pursuit defect need not be total. Decreased smooth pursuit gain ipsilateral to the side of cortical ablation and increased contralateral pursuit gain are manifested by nystagmus that beats toward the damaged cerebral hemisphere [4]. Pursuit paretic nystagmus can be explained by imbalanced pursuit system input to the pontine neural integrators that are presumed to reciprocally maintain horizontal eye position in response to pursuit, saccadic, or vestibular signals [3]. Linear slow phases distinguish this pursuit paretic nystagmus 141 from the gaze paretic nystagmus of posterior fossa disease, which has decreasing velocity exponential slow phases and occurs only during eccentric gaze [21.
Jack N. Alpert, M D The interesting report by D r Abel and colleagues presents the first case of horizontal pursuit defect nystagmus [l]. They acknowledge that one characteristic of this nystagmus is “lack of substantive changes in darkness.” Yet in Figure 2B, quick-phase velocity and nystagmus amplitude both increased. Their patient showed a linear slow phase that “did not increase in velocity during Jarkness.” Although frequency of nystagmus decreased, the tracing shows what appears to be a steeper slope of the slow phases in darkness. Perhaps this is not the case, but without direct measurement of slow-phase velocity, it is hard to make a convincing case for pursuit defect nysragmus. In 2 clinical reports of upbeat and downbeat pursuit defect nystagmus, eye movement tracings clearly showed either no change or abolition of nystagmus with loss of visual fixation [2, 31. Clinically, their patient had severe left-sided hearing loss, a diminished left corneal response. left facial paresis, and left hemiataxia. This constellation o f findings suggests the possibility of vestibular involvement on the left as well. Caloric studies were not reported. Was there a canal paresis on the left? The vestibuloocular reflexes with rotation in a Barany chair shown in Figure 5B are asymmetrical, with movement to the left better than to the right. Unless normal left eighth nerve function is proved, it is hard to be certain that this is a case of horizontal pursuit defect nystagmus.
References 1. Abel LA, Daroff RB, Dell’Osso LF: Horizontal pursuit defect nystagmus. Ann Neurol 5:449-452, 19’9 2. Alpert J: Downbeat nystagmus due to ariticonvulsanr toxicity. A n n Neurol 4:471-473, 1978 3. Gilman N , Baloh RW, Tomiyasu U: Primary position upbeat nystagmus. Neurology (Minneap) 27:29-298, 19:-
Address reprint requests to Dr Alpert, Hermann Professional Bldg, Suite 910, Houston, T X 77030.
References 1. Abel LA, Daroff RB, Dell’Osso LF: Horizontal pursuit defect nystagmus. Ann Neurol 5:449-452, 1979 2. Daroff RB, Troost BT, Dell’Osso LF: Nystagmus and other ocular oscillations, in Glaser JS (ed): Neuro-ophthalmology. Hagerstown, MD, Harper & Row, 1978, p p 219-240 3. Robinson DA: Oculomotor control signals, in Lennerstrand G , Bach y Rita P ieds): Basic Mechanisms of Ocular Motility and Their Clinical Implications. New York, Pergamon, 1975, pp
Reply Robert B. Daroff, MD, Louis F. Dell’Osso, PhD, and Larry A. Abel, P h D
317-374 4. Sharpe JA, 1.0 AW, Rabinovitch HE: Control of the saccadic
D r Sharpe’s important finding of horiLonta1 pursuit defect nystagmus in hemispherectomized patients demonstrates that the defect need not be absolute to produce a nystagmus-inducing imbalance. So prompted, we inspected
From the Neuro-ophthalmology Unit, Division of Neurology, Toronto Western Hospital, University of Toronto, 399 Bathurst St, Toronto, Ont, Canada MST 2%.
From the Ocular Motor Neurophysiology Laboratory, Miami Veterans Administration Medical Center, anci the Department of Neurology, University of Miami School of hledicine, Miami, FL.
458 Annals of Neurology Vol 6 No 5
November 1979
and smooth pursuit systems after cerebral hemidecortication. Brain 102:387-403, 1979 5 . Z e e DS, Friendlich AR, Robinson DA: The mechanism of downbeat nystagmus. Arch Neurol 30:227-237, 197‘1
James A. Sharpe, M D
Left Vestibular Involvement Primary-position horizontal jerk nystagmus with linear slow phases is typically caused by vestibular imbalance. Primary-position vertical jerk nystagmus is caused by vertical imbalance in the smooth pursuit system [ 5 ] , be it downbeating or upbeating [2]. The nystagmus beats in the direction of impaired pursuit. The report by Drs Abel, Daroff, and Dell’Osso [ 11 described primary-position horizontal jerk nystagmus in a patient with a posterior fossa tumor. The nystagmus had linear slow phases and exhibited the following features that distinguished it from vestibular nystagmus [ 51: ( 1) failure of the nystagmus slow-phase velocity to increase in darkness; (2) unidirectional impairment of pursuit in the direction of the fast phase; and (3) bidirectional preservation of the vestibuloocular reflex. The authors commented that such nystagmus does not accompany the pursuit paresis occurring ipsilateral to unilateral cerebral hemispheric lesions. They speculated that cerebral disease does not cause nystagmus, either because the brainstem and cerebellum are intact, o r because cerebral damage causes paresis of pursuit, not total paralysis. I wish to point out that unilateral cerebral damage can cause primary-position horizontal jerk nystagmus. In our laboratory, pursuit paretic nystagmus was identified in each of 5 patients studied eight to twelve years after cerebral hemidecortication [4]. Clinical and radiological examination indicated intact cerebellar and brainstem function. The pursuit defect need not be total. Decreased smooth pursuit gain ipsilateral to the side of cortical ablation and increased contralateral pursuit gain are manifested by nystagmus that beats toward the damaged cerebral hemisphere [4]. Pursuit paretic nystagmus can be explained by imbalanced pursuit system input to the pontine neural integrators that are presumed to reciprocally maintain horizontal eye position in response to pursuit, saccadic, or vestibular signals [3]. Linear slow phases distinguish this pursuit paretic nystagmus 141 from the gaze paretic nystagmus of posterior fossa disease, which has decreasing velocity exponential slow phases and occurs only during eccentric gaze [21.
Jack N. Alpert, M D The interesting report by D r Abel and colleagues presents the first case of horizontal pursuit defect nystagmus [l]. They acknowledge that one characteristic of this nystagmus is “lack of substantive changes in darkness.” Yet in Figure 2B, quick-phase velocity and nystagmus amplitude both increased. Their patient showed a linear slow phase that “did not increase in velocity during Jarkness.” Although frequency of nystagmus decreased, the tracing shows what appears to be a steeper slope of the slow phases in darkness. Perhaps this is not the case, but without direct measurement of slow-phase velocity, it is hard to make a convincing case for pursuit defect nysragmus. In 2 clinical reports of upbeat and downbeat pursuit defect nystagmus, eye movement tracings clearly showed either no change or abolition of nystagmus with loss of visual fixation [2, 31. Clinically, their patient had severe left-sided hearing loss, a diminished left corneal response. left facial paresis, and left hemiataxia. This constellation o f findings suggests the possibility of vestibular involvement on the left as well. Caloric studies were not reported. Was there a canal paresis on the left? The vestibuloocular reflexes with rotation in a Barany chair shown in Figure 5B are asymmetrical, with movement to the left better than to the right. Unless normal left eighth nerve function is proved, it is hard to be certain that this is a case of horizontal pursuit defect nystagmus.
References 1. Abel LA, Daroff RB, Dell’Osso LF: Horizontal pursuit defect nystagmus. Ann Neurol 5:449-452, 19’9 2. Alpert J: Downbeat nystagmus due to ariticonvulsanr toxicity. A n n Neurol 4:471-473, 1978 3. Gilman N , Baloh RW, Tomiyasu U: Primary position upbeat nystagmus. Neurology (Minneap) 27:29-298, 19:-
Address reprint requests to Dr Alpert, Hermann Professional Bldg, Suite 910, Houston, T X 77030.
References 1. Abel LA, Daroff RB, Dell’Osso LF: Horizontal pursuit defect nystagmus. Ann Neurol 5:449-452, 1979 2. Daroff RB, Troost BT, Dell’Osso LF: Nystagmus and other ocular oscillations, in Glaser JS (ed): Neuro-ophthalmology. Hagerstown, MD, Harper & Row, 1978, p p 219-240 3. Robinson DA: Oculomotor control signals, in Lennerstrand G , Bach y Rita P ieds): Basic Mechanisms of Ocular Motility and Their Clinical Implications. New York, Pergamon, 1975, pp
Reply Robert B. Daroff, MD, Louis F. Dell’Osso, PhD, and Larry A. Abel, P h D
317-374 4. Sharpe JA, 1.0 AW, Rabinovitch HE: Control of the saccadic
D r Sharpe’s important finding of horiLonta1 pursuit defect nystagmus in hemispherectomized patients demonstrates that the defect need not be absolute to produce a nystagmus-inducing imbalance. So prompted, we inspected
From the Neuro-ophthalmology Unit, Division of Neurology, Toronto Western Hospital, University of Toronto, 399 Bathurst St, Toronto, Ont, Canada MST 2%.
From the Ocular Motor Neurophysiology Laboratory, Miami Veterans Administration Medical Center, anci the Department of Neurology, University of Miami School of hledicine, Miami, FL.
458 Annals of Neurology Vol 6 No 5
November 1979
