Parietal and occipital seizures have been investigated relatively litt
le. Recent interest in seizures of frontal lobe origin has led to a de
finition of several well-identifiable clinical patterns of frontal lob
e seizures. A similar delineation of the clinical and EEG pattern of p
arietal and occipital epilepsy, using modern investigations, appears a
ppropriate, not least because the few reported series of surgical trea
tment in parietal and occipital epilepsy have indicated that operation
may be relevant in selected cases, not only for removal of space-occu
pying lesions. Such a study is currently being undertaken at the Natio
nal Hospital for Neurology and Neurosurgery and The Chalfont Centre fo
r Epilepsy with the aim of developing and evaluating diagnostic criter
ia for these seizures. From the existing literature we can conclude th
at precise incidence and prevalence are largely unknown. A recent comm
unity-based study of 252 subjects with partial epileptic seizures in a
n epileptic population of 594, showed that parietal seizures and seizu
res of posterior origin each comprised 6.3% and central or sensory-mot
or seizures comprised 32.5% of focal seizures in the 160 cases in whic
h seizures could be subclassified (Manford et al., 1992). This inciden
ce seems low for occipital seizures as compared with the 1953 study by
Gibbs and Gibbs, who observed occipital epileptiform activity in 8% o
f subjects with focal epilepsy. The most prominent clinical manifestat
ions of parietal epilepsy are elementary sensory phenomena at the begi
nning of seizures and elementary visual hallucinations in occipital ep
ilepsy. These symptoms are not associated solely with posterior hemisp
here epilepsy, however, and more studies are obviously needed to defin
e how close this relation is. Scalp EEG is frequently negative or mayb
e misleading; furthermore, spread of epileptic discharges from the par
ietal and occipital lobes to frontal and temporal regions may obscure
seizure origin. Because of these controversial symptoms, diagnostic cr
iteria may be difficult to define. The wide difference in clinical and
EEG manifestations between reported series of parietal and occipital
epilepsy also reflects a considerable problem with patient sampling. C
lassification of epilepsy according to the anatomic division of the br
ain may be arbitrary, and it may be appropriate to define epileptic sy
ndromes such as sensorimotor seizures or occipitotemporal seizures tha
t cross such artificial divides.