Limits...
Epileptic monocular nystagmus and ictal diplopia as cortical and subcortical dysfunction.

Schulz R, Tomka-Hoffmeister M, Woermann FG, Hoppe M, Schittkowski MP, Ebner A, Bien CG - Epilepsy Behav Case Rep (2013)

Bottom Line: Interictal neuroophthalmological examination showed several beats of a monocular nystagmus and a spasm of the contralateral eye.An exclusively ictal monocular epileptic nystagmus could be an argument for an exclusively cortical involvement in monocular eye movement control.The interictal findings in our patient, however, argue for an irregular ictal activation of both the cortical frontal eye field and the brainstem.

View Article: PubMed Central - PubMed

Affiliation: Epilepsie-Zentrum Bethel, Krankenhaus Mara, Maraweg 21, D-33617 Bielefeld, Germany.

ABSTRACT
We present the case of a patient with ictal monocular nystagmus and ictal diplopia who became seizure-free after resection of a right frontal focal cortical dysplasia (FCD), type 2B. Interictal neuroophthalmological examination showed several beats of a monocular nystagmus and a spasm of the contralateral eye. An exclusively ictal monocular epileptic nystagmus could be an argument for an exclusively cortical involvement in monocular eye movement control. The interictal findings in our patient, however, argue for an irregular ictal activation of both the cortical frontal eye field and the brainstem.

No MeSH data available.


Related in: MedlinePlus

Hypothesis of brain stem involvement in epileptic monocular nystagmus. A: EEG: channels FP1-F7, F7-T7, and IO1-PZ (left infraorbital) show an eye artifact by monocular nystagmus of the left eye, with evolution of frequency (initially 7 Hz, later 4 Hz); vertical arrow; the EEG with reference PZ shows most prominent deflections in F7 and IO1 which indicate an additional vertical component of the rapid monocular eye movements (Supplemental material). From second 5 on, a rapid EEG seizure pattern evolves over the right frontocentral region (phase reversal at channel F4-C4; horizontal arrow). B: Pre- and postoperative MRI (coronal und transversal planes); white arrows indicate the right frontal focal cortical dysplasia. C: Hypothesis for brainstem involvement: a) Usual ictal activation: right frontal cortical seizure activity (FEF = frontal eye field; dark red) propagates to the contralateral left paramedian pontine reticular formation (PPRF), nucleus nerve VI (nc.VI), and via the right medial longitudinal fasciculus (MLF) to the contralateral right nucleus nerve III (nc.III), with subsequent activation of the lateral rectus muscle of the left eye (LR) and the medial rectus muscle of the right eye (MR); effect: gaze of both eyes to the left. b) Irregular ictal activation: in addition, activation of the left nc.III; effect: coactivation of the medial and lateral rectus muscles of the left eye, with left monocular nystagmus, strabismus, and diplopia (D). The comparatively wide left palpebral fissure could result from innervation of the levator palpebrae muscle of the left eye (innervation by the 3rd nerve, n.III). Usual plus irregular ictal brainstem activation is marked in dark magenta. c) Irregular interictal state (bright magenta): ictal dysfunction with predominance of the left brainstem is followed by residual dysfunction of the right nc.VI and nc.VII. This results in a net hyperfunction of the right n.VI with monocular lateral nystagmus of the right eye and involves the right n.VII with right periocular spasm (E). For further illustrations, see also the videos in the Supplemental material. The dysfunction of the brainstem ceased after successful right frontal cortical epilepsy surgery and neuroophthalmological findings normalized.
© Copyright Policy - CC BY-NC-ND
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4150613&req=5

f0005: Hypothesis of brain stem involvement in epileptic monocular nystagmus. A: EEG: channels FP1-F7, F7-T7, and IO1-PZ (left infraorbital) show an eye artifact by monocular nystagmus of the left eye, with evolution of frequency (initially 7 Hz, later 4 Hz); vertical arrow; the EEG with reference PZ shows most prominent deflections in F7 and IO1 which indicate an additional vertical component of the rapid monocular eye movements (Supplemental material). From second 5 on, a rapid EEG seizure pattern evolves over the right frontocentral region (phase reversal at channel F4-C4; horizontal arrow). B: Pre- and postoperative MRI (coronal und transversal planes); white arrows indicate the right frontal focal cortical dysplasia. C: Hypothesis for brainstem involvement: a) Usual ictal activation: right frontal cortical seizure activity (FEF = frontal eye field; dark red) propagates to the contralateral left paramedian pontine reticular formation (PPRF), nucleus nerve VI (nc.VI), and via the right medial longitudinal fasciculus (MLF) to the contralateral right nucleus nerve III (nc.III), with subsequent activation of the lateral rectus muscle of the left eye (LR) and the medial rectus muscle of the right eye (MR); effect: gaze of both eyes to the left. b) Irregular ictal activation: in addition, activation of the left nc.III; effect: coactivation of the medial and lateral rectus muscles of the left eye, with left monocular nystagmus, strabismus, and diplopia (D). The comparatively wide left palpebral fissure could result from innervation of the levator palpebrae muscle of the left eye (innervation by the 3rd nerve, n.III). Usual plus irregular ictal brainstem activation is marked in dark magenta. c) Irregular interictal state (bright magenta): ictal dysfunction with predominance of the left brainstem is followed by residual dysfunction of the right nc.VI and nc.VII. This results in a net hyperfunction of the right n.VI with monocular lateral nystagmus of the right eye and involves the right n.VII with right periocular spasm (E). For further illustrations, see also the videos in the Supplemental material. The dysfunction of the brainstem ceased after successful right frontal cortical epilepsy surgery and neuroophthalmological findings normalized.

Mentions: A right-handed 36-year-old man had video-EEG monitoring in our epilepsy surgery program. Since the age of 16, this patient had seizures 30 times a day, with turning of the head and asymmetric gaze shift of both eyes to the left, more prominent of the adducting right than of the abducting left eye, with resulting strabismus convergens and complaint of diplopia, accompanied by a 4- to 8-Hz prominent leftward nystagmus of the left eye. Noninvasive and invasive video-EEG monitoring documented seizure origin from a right frontal lesion (focal cortical dysplasia (FCD) type 2B by MRI criteria; Fig. 1). The patient was seizure-free subsequent to extended resection of the right frontal lesion with the histopathological diagnosis of FCD 2B, with a follow-up of 1 1/2 years so far.


Epileptic monocular nystagmus and ictal diplopia as cortical and subcortical dysfunction.

Schulz R, Tomka-Hoffmeister M, Woermann FG, Hoppe M, Schittkowski MP, Ebner A, Bien CG - Epilepsy Behav Case Rep (2013)

Hypothesis of brain stem involvement in epileptic monocular nystagmus. A: EEG: channels FP1-F7, F7-T7, and IO1-PZ (left infraorbital) show an eye artifact by monocular nystagmus of the left eye, with evolution of frequency (initially 7 Hz, later 4 Hz); vertical arrow; the EEG with reference PZ shows most prominent deflections in F7 and IO1 which indicate an additional vertical component of the rapid monocular eye movements (Supplemental material). From second 5 on, a rapid EEG seizure pattern evolves over the right frontocentral region (phase reversal at channel F4-C4; horizontal arrow). B: Pre- and postoperative MRI (coronal und transversal planes); white arrows indicate the right frontal focal cortical dysplasia. C: Hypothesis for brainstem involvement: a) Usual ictal activation: right frontal cortical seizure activity (FEF = frontal eye field; dark red) propagates to the contralateral left paramedian pontine reticular formation (PPRF), nucleus nerve VI (nc.VI), and via the right medial longitudinal fasciculus (MLF) to the contralateral right nucleus nerve III (nc.III), with subsequent activation of the lateral rectus muscle of the left eye (LR) and the medial rectus muscle of the right eye (MR); effect: gaze of both eyes to the left. b) Irregular ictal activation: in addition, activation of the left nc.III; effect: coactivation of the medial and lateral rectus muscles of the left eye, with left monocular nystagmus, strabismus, and diplopia (D). The comparatively wide left palpebral fissure could result from innervation of the levator palpebrae muscle of the left eye (innervation by the 3rd nerve, n.III). Usual plus irregular ictal brainstem activation is marked in dark magenta. c) Irregular interictal state (bright magenta): ictal dysfunction with predominance of the left brainstem is followed by residual dysfunction of the right nc.VI and nc.VII. This results in a net hyperfunction of the right n.VI with monocular lateral nystagmus of the right eye and involves the right n.VII with right periocular spasm (E). For further illustrations, see also the videos in the Supplemental material. The dysfunction of the brainstem ceased after successful right frontal cortical epilepsy surgery and neuroophthalmological findings normalized.
© Copyright Policy - CC BY-NC-ND
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4150613&req=5

f0005: Hypothesis of brain stem involvement in epileptic monocular nystagmus. A: EEG: channels FP1-F7, F7-T7, and IO1-PZ (left infraorbital) show an eye artifact by monocular nystagmus of the left eye, with evolution of frequency (initially 7 Hz, later 4 Hz); vertical arrow; the EEG with reference PZ shows most prominent deflections in F7 and IO1 which indicate an additional vertical component of the rapid monocular eye movements (Supplemental material). From second 5 on, a rapid EEG seizure pattern evolves over the right frontocentral region (phase reversal at channel F4-C4; horizontal arrow). B: Pre- and postoperative MRI (coronal und transversal planes); white arrows indicate the right frontal focal cortical dysplasia. C: Hypothesis for brainstem involvement: a) Usual ictal activation: right frontal cortical seizure activity (FEF = frontal eye field; dark red) propagates to the contralateral left paramedian pontine reticular formation (PPRF), nucleus nerve VI (nc.VI), and via the right medial longitudinal fasciculus (MLF) to the contralateral right nucleus nerve III (nc.III), with subsequent activation of the lateral rectus muscle of the left eye (LR) and the medial rectus muscle of the right eye (MR); effect: gaze of both eyes to the left. b) Irregular ictal activation: in addition, activation of the left nc.III; effect: coactivation of the medial and lateral rectus muscles of the left eye, with left monocular nystagmus, strabismus, and diplopia (D). The comparatively wide left palpebral fissure could result from innervation of the levator palpebrae muscle of the left eye (innervation by the 3rd nerve, n.III). Usual plus irregular ictal brainstem activation is marked in dark magenta. c) Irregular interictal state (bright magenta): ictal dysfunction with predominance of the left brainstem is followed by residual dysfunction of the right nc.VI and nc.VII. This results in a net hyperfunction of the right n.VI with monocular lateral nystagmus of the right eye and involves the right n.VII with right periocular spasm (E). For further illustrations, see also the videos in the Supplemental material. The dysfunction of the brainstem ceased after successful right frontal cortical epilepsy surgery and neuroophthalmological findings normalized.
Mentions: A right-handed 36-year-old man had video-EEG monitoring in our epilepsy surgery program. Since the age of 16, this patient had seizures 30 times a day, with turning of the head and asymmetric gaze shift of both eyes to the left, more prominent of the adducting right than of the abducting left eye, with resulting strabismus convergens and complaint of diplopia, accompanied by a 4- to 8-Hz prominent leftward nystagmus of the left eye. Noninvasive and invasive video-EEG monitoring documented seizure origin from a right frontal lesion (focal cortical dysplasia (FCD) type 2B by MRI criteria; Fig. 1). The patient was seizure-free subsequent to extended resection of the right frontal lesion with the histopathological diagnosis of FCD 2B, with a follow-up of 1 1/2 years so far.

Bottom Line: Interictal neuroophthalmological examination showed several beats of a monocular nystagmus and a spasm of the contralateral eye.An exclusively ictal monocular epileptic nystagmus could be an argument for an exclusively cortical involvement in monocular eye movement control.The interictal findings in our patient, however, argue for an irregular ictal activation of both the cortical frontal eye field and the brainstem.

View Article: PubMed Central - PubMed

Affiliation: Epilepsie-Zentrum Bethel, Krankenhaus Mara, Maraweg 21, D-33617 Bielefeld, Germany.

ABSTRACT
We present the case of a patient with ictal monocular nystagmus and ictal diplopia who became seizure-free after resection of a right frontal focal cortical dysplasia (FCD), type 2B. Interictal neuroophthalmological examination showed several beats of a monocular nystagmus and a spasm of the contralateral eye. An exclusively ictal monocular epileptic nystagmus could be an argument for an exclusively cortical involvement in monocular eye movement control. The interictal findings in our patient, however, argue for an irregular ictal activation of both the cortical frontal eye field and the brainstem.

No MeSH data available.


Related in: MedlinePlus