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|LETTER TO EDITOR
|Year : 2015 | Volume
| Issue : 2 | Page : 262-264
Unilateral spatial neglect as a presenting manifestation of nonconvulsive status epilepticus
Rohan Mahale, Anish Mehta, R Srinivasa
Department of Neurology, Mathikere Sampangappa Ramaiah Medical College and Hospital, Bangalore, Karnataka, India
|Date of Web Publication||5-May-2015|
Department of Neurology, Mathikere Sampangappa Ramaiah Medical College and Hospital, Bangalore, Karnataka
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Mahale R, Mehta A, Srinivasa R. Unilateral spatial neglect as a presenting manifestation of nonconvulsive status epilepticus. Neurol India 2015;63:262-4
Nonconvulsive status epilepticus (NCSE) is defined as a change in the mental status of at least 30 to 60 minutes duration, associated with continuous or near continuous ictal discharges detectable on an electroencephalography (EEG).  A diagnosis of NCSE requires the clinical manifestation of an abnormal mental status with reduced responsiveness, a supportive EEG, and a response to an antiepileptic drug. Unilateral spatial neglect (USN) as a manifestation of NCSE has not been reported till date. Here, we report the case of an elderly gentleman who presented with left spatial neglect with his EEG showing continuous, sharp wave discharges from the right parietooccipital region suggestive of the background presence of a NCSE.
A 64-year-old, right-handed man was brought in an altered mental status of a day's duration. His wife found him to be in an acute confusional state on being woken up. He was talking irrelevantly and was disoriented. He was always looking towards his right side and was not moving his left upper and lower limb spontaneously and to any painful stimulus. On admission, he was drowsy but easily arousable on verbal commands. A command to shift his gaze towards his left side would make him look towards the right side. There was intermittent horizontal, jerky nystagmus of both eyes towards the left side with fast component also towards the left. Several requests to lift his left upper and lower limbs always resulted in his lifting his right upper and lower limb. If the examiner called his name from his left hemispace, he would respond by looking towards his right hemispace [Video 1 (www.neurologyindia.com)]. There was no facial palsy. He had a normal tone, power and reflexes in his limbs with flexor plantars. His magnetic resonance imaging (MRI) of the brain showed diffusion restriction in the right parieto-temporo-occipital region with a hyperintense signal change in the right pulvinar region of the thalamus on fluid-attenuated inversion recovery (FLAIR) images [Figure 1]. The MR angiography was normal. His EEG showed sharp wave discharges from the right temporo-parieto-occipital region with generalization, which disappeared on intravenous lorazepam (4mg) administration suggesting the presence of a NCSE [Figure 2]. His cerebrospinal fluid (CSF) analysis was normal and the CSF polymerase chain reaction (PCR) for herpes simplex virus was negative. A diagnosis of left USN as a manifestation of NCSE was made. He was treated with a loading dose of intravenous phenytoin (20 mg/kg) followed by continuance of a maintenance dose (5 mg/kg). A repeat EEG performed after 48 h revealed the disappearance of the epileptiform discharges. There was clinical improvement in the form of disappearance of the spatial neglect with return to normal sensorium [Video 2 (www.neurologyindia.com)].
|Figure 1: (a-d) Magnetic resonance imaging (MRI) brain diffusion-weighted MRI (DWI) images axial view showing gyral hyperintensities in the right parieto-temporo-occipital region and right pulvinar of thalamus (white arrow); (e-g) MRI brain apparent-diffusion coefficient (ADC) showing corresponding hypointensities indicating diffusion restriction (white arrow)|
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|Figure 2: Electroencephalogram (EEG) (bipolar longitudinal montage, sensitivity 14.0 μV/mm, low frequency filter 1 Hz, high frequency filter 70 Hz, notch 50 Hz, and speed 30 mm/s) showing sharp wave discharges from the right temporo-parieto-occipital region (red arrow) and disappearance of discharges with intravenous lorazepam|
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NCSE constitutes approximately 20-23% of cases presenting as status epilepticus. The clinical presentation of a NCSE may vary from manifesting as a subtle abnormality to the presence of one or more of the following: Variation in the level of consciousness, fluctuation in behavior, semi-purposeful movements, changes in or even a loss of speech, or uncontrolled jerky movements of the face, mouth or limbs. USN as a manifestation of NCSE has not been reported till date.
USN is a common finding in patients with a right hemispheric stroke and is defined as "the failure to report, respond, or orient to novel or meaningful stimuli presented to the side opposite a brain lesion, when this failure cannot be attributed to either sensory or motor defects."  It is a failure or decreased ability to move in the contra- lesional space despite being aware of a stimulus in that space. Normally, the right hemisphere attends to both hemispaces, while the left hemisphere attends primarily to the right hemispace. In a right hemispheric lesion, the left hemisphere attends primarily to the right hemispace resulting in a neglect of the left hemispace. 
USN occurs as a result of lesions at the parietooccipital junction in the right hemisphere.  But, lesions in the occipital and frontal lobes, the thalamus, and putamen can also produce this symptom. Valler et al., (1988) suggested that the right fronto-temporo-parietal cortex could be the site of the lesion responsible for the USN.  Mesulam suggested that the posterior parietal, frontal, and reticular components provide an integrated network for the modulation of attention within the extrapersonal space.  The posterior parietal lobe is primarily responsible for creating a sensory representation of extrapersonal events, and for targeting specific stimuli. The frontal eye fields and adjacent premotor areas regulate visual scanning, orient the head and eyes to explore the environment, and initiate motor acts for limb movement. Each component region gives rise to a different clinical type of USN when damaged. Transient regional diffusion-weighted MRI (DWI) hyperintensity has been reported in patients with status epilepticus. MRI abnormalities in our patient may have, in all probability, been due to NCSE, since the CSF examination and angiography were normal.
To conclude, this patient had a left unilateral spatial motor neglect as an ictal manifestation with the EEG showing epileptiform discharges. The motor neglect disappeared following the administration of an appropriate antiepileptic drug. NCSE should be considered as an etiology for causing USN apart from the usual vascular lesions.
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[Figure 1], [Figure 2]
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