Cases with parietal and occipital lobe epilepsies

The female patient 37 years of age suffered since her 3rd year of life from a pharmacoresistent focal epilepsy with different seizure types. Focal aware seizures with sudden visual disturbance, semiology later during the seizure epigastric aura, vertigo-nausea, headache temple right, duration 1–4 min, frequency 12 times per month, focal unaware seizures with or without stare gaze, oral automatisms, no reaction, memory impairment, in 50% of these seizures involvement to bilateral tonic-clonic seizures occurred.

MEG detected interictal spikes, source localization indicated focal epileptic activity parietal right (Fig. 1a, b + c).

A male patient, age 37 years old, focal epilepsy since 7th year of life, pharmacoresistent.

MRI detected a lesion parietal left (Fig. 2).

Fifteen years old female patient, suffering from seizures since her 7th years of life, pharmacoresistent focal epilepsy, in childhood leukemia, sinus vein thrombosis.

Semiology: Focal aware seizures: a dark spot occurring in the left visual field, sometimes anxiety during seizures (leading to the suspicion of non-epileptic psychogenic pseudoseizures), duration: seconds to minutes, frequency: several times per day.

Neurological examination and surface EEG were normal. During video EEG recording the patient reported seeing a “spot” in the visual field left. A seizure occurred. Simultaneously while seeing a spot in the left visual field in the ictal EEG seizure onset occurred occipital right (Fig. 3).

MRI demonstrated an atrophy occipito-temporal right after sinus vein thrombosis (Fig. 4).

The EEG shows rapid propagation from parietal to temporal lobe. Vertigo provides a semiological hint for extratemporal seizure onset. The other ictal signs could lead to the wrong diagnosis of temporal lobe epilepsy. Non-invasive source localization by means of MEG/EEG strengthens the semiology based hypothesis of parietal focus with propagation to temporal and was used for guidance of invasive electrode implantation.

The aura can be interpreted as related to a kind of “out of body experience”, being localized to the parietal lobe. MRI and MEG confirmed the localization of epileptic activity in this area. In case of normal MRI postprocessing with morphometric analysis program (MAP) enables in some patients to detect “hidden” FCD II lesions in MRI. In this patient MRI showed the lesion already without MAP.

MRI showed a widespread atrophy after sinus vein thrombosis only. The clinical phenomenology suggested posterior cortex epilepsy. Anxiety during the seizure raised the question of non-epileptic attacks. Temporal lobe epilepsy or non-epileptic panic attacks were ruled out by ictal video-EEG recordings demonstrating a focal seizure onset in the occipital lobe during seizure onset with following propagation.

Compared to temporal or frontal lobe epilepsies parietal (PLO) and occipital lobe (OLE) epilepsies occur rarely. The occurrence for PLO is reported wih 5–8% und for OLE 1.5–8% [1‐6]. Parietal (PLO) and occipital lobe(OLE) epilepsies are condensed as epilepsy of the posterior cortex.

Case 1 and 2 are diagnosed as parietal lobe epilepsies. In addition to the presentation of cases with clinical findings, characteristics of parietal epilepsies concerning ictal semiology, electrophysiology and imaging are discussed.

a) Seizure semiology

During epileptic nystagmus the fast component beats to the side contralateral to the focus. Parietal cortical stimulation during stereo-EEG-registration showed that the body scheme disturbances were only triggered in the non-dominant hemisphere whereas sensoric illusions or hallucinations as well as eyes/eyelid movements or sensations significantly cohered with the stimulation of the intraparietal sulcus [7]. Somatosensory sensations including motoric symptoms und dysarthria were detectable at stimulation of the postcentral gyrus. The “second sensory area”, the left parietal opercula is involved in the supralaryngeal control. Ictal extremity agnosia and phantom extremity arise in der posterior parietal brain region. The neglect more often is associated with a right excitation of the inferior parietal brain. “Out-of-body experiences” are due to parieto-temporal excitations [8].

Because during parietal lobe seizures occur bilateral somatosensoric illusions combined with vertigo, disturbances of body scheme and only mild motoric signs (tremor, dyspractic movements), but with prominent emotional components such as fear or panic can be mistaken as psychogenic non-epileptic seizures.

b) EEG

During focal unaware seizures the surface EEG may show no unambiguous epileptiform activity. Because of rapid propagation surface EEG in many patients is not sufficient for localization of the focal epileptic activity. Source localization by means of MEG/EEG can provide improved information. In case of FCD type II related epilepsy MEG showed excellent surgical outcomes [9]. When MRI turns out as normal then propagated epileptic activity in a late phase of a seizure may be wrongly diagnosed as seizure onset region. Propagation is found frequently from parietal to temporal or frontal brain regions [3]. An invasive study was performed in 37 of the 38 patients for epilepsy surgery [10]. Seizure disappeared in 15 (Engel’s classification I, 39.5%), and rare seizure remained in 5 (Engel II, 13.2%). Thirteen patients showed a worthwhile improvement (Engel III, 34.2%), whereas 5 exhibited no worthwhile improvement (Engel IV, 13.2%).

c) Imaging

MRI showed abnormal findings in 68%. MRI detected in 36.8% parietal lesions (28.95% unilateral), hippocampal atrophy in 10.5%, other atrophies 10.5% [10]. Most common cortical dysplasia was detected by histology in these operated patients. Of 39 patients seizures disappeared postoperatively in 39.5% (Engel class I) and rare seizure remained in 13.2% (Engel class II). 34.2% of the patients showed a worthwhile improvement (Engel class III), whereas 13.2% exhibited no worthwhile improvement (Engel class IV).

A meta-analysis of 253 operated patients (postoperative follow up 104.9 + 74.8 months) showed Engel Class 1 in 62.4% [11].

d) Etiology

Histopathological findings of pharmacoresistent parietal lobe epilepsies were collected at the neuropathology reference center for epilepsy surgery Erlangen. In the resected brain tissue specimens after epilepsy surgery of 126 patients the following lesions were detected by histopathological examination: FCD II 17.8%, glial scar 14.1%, diffuse glioma 13.3%, ganglioglioma 12.6%, DNT 9.6%, FCD not otherwise specified (NOS) 9.6%), cavernoma 6.7%, FCD1 6.7%, no lesion 8.3%, vascular malformation 4.4% [12].

Case 3 was diagnosed as occipital lobe epilepsy. Characteristic findings of occipital lobe epilepsies are as follows.

a) Seizure semiology

Ictal clinical signs are mainly visual and oculomotor. Often elementary visual hallucinations and postictal headache exist.

Visual phenomena build a functional link between parietal occipital lobe epilepsy: epileptic discharges from parieto-occipital transition region or occipital brain region may produce ictal visual phenomena. Elementary visual hallucinations are simple light sensations, colored spot, ring, occasionally with transient amaurosis contralateral to the seizure onset. Visual iIlusions can also be simply colour changes of objects.

Visual illusion or loss of vision not only exist in occipital lobe epilepsies, but also in occipito-temporal or even antero-temporal seizures. Complex hallucinations were not observed in occipital lobe patients [13]. Motoric ictal signs are lid blinking and contralateral eye movements. For visual processing two streams are differentiated:

Fast propagation to frontal (30%) or temporal (30%) can overshadow it [3, 4]. In case of reagibility of the patient this speaks in favour of onset in the calcarine area, if not then for onset in the temporo-occipital area. Ictal signs don’t permit the definite differentiation of mesial or lateral occipital seizure onset [14].

The differential diagnosis of idiopathic occipital childhood epilepsy concerns mainly symptomatic occipital epilepsy and migraine. Elementary visual hallucinations of occipital seizures in idiopathic epilepsy develop rapidly within seconds, are brief in duration (2–3 min), frequent, usually colored and circular, whereas in case of migraine an aura slowly arises lasting ≥5 min and is mostly uncolored with linear shapes. In the Panayiotopoulus syndrome seizures occur with autonomic signs, the duration is longer and if visual symptoms exist they are not the only ictal manifestation.

b) Imaging

MRI detects like in parietal lobe epilepsy structural changes and provides important information for the localization hypothesis of the epileptogenic area.

cortical dysplasia 5/26, cerebromalacia 5/26, DNET, ganglioglioma calcification, infarction each 1/26 in the epilepsy surgery report from Sang Kun Lee et al. 2005 [15]. MRI correctly localized the lesion in seven of 16 (43.7%) postoperative seizure-free patients, FDG-PET in 50%, ictal SPECT in 25%.

c) EEG

EEG interictally shows unilateral posterior EEG slowing more common than occipital spikes.

In photosensitive OLE during intermittent photic stimulation spikes/polyspikes occipital or generalized spikes/polyspikes with posterior accentuation are recorded [5]. The interictal EEG often shows spikes which rarely are correctly localized in the occipital lobe, but more often posterior temporal. In the ictal EEG epileptiform pattern may be missed or mislead the localization of seizure onset due to propagation to bilateral occipital or temporal regions. Source localization in MEG/EEG combined with MRI (MSI) are helpful for implantations of invasive electrodes.

Epilepsy surgery results are reported only in small numbers. Postoperative seizure free were 61.5% in 26 operated patients [15].

d) Etiology

Histopathological findings of patients with operated pharmacoresistent occipital lobe epilepsies showed in the resected brain tissue specimens similar lesion as in the parietal lobe epilepsies.