It was perhaps Penfield and his colleagues who initially discussed in some detail the issue of postoperative neurological deficits following resective surgery for the management of intractable epilepsy. Their observations were undertaken in the early half of the twentieth century, long before the introduction of the quality imaging that might have added significant certainty to what was empirically considered to be the etiology of such deficits. The term “neuroparalytic edema” was coined by Penfield and was thought to be a significant cause of the deficits; it was considered to be an edematous swelling of cerebral parenchyma in the vicinity of the cortical excisions and was usually transient (1958). Penfield felt that it was at least partially related to the duration of the operative exposure of the cortex. He considered that the clinical symptomatology consisted of headache, paresis, focal (“neighborhood”) seizures, dysphasia, etc. These were usually transient, reaching their peak during the initial 5 days and then gradually declining. There have been a number of discussions related to the possible explanations of Dr. Penfield’s “neuroparalytic edema,” but none has been accepted as a consensus. It is not now considered, if indeed it occurs, as a complication!

Penfield also described aseptic meningitis as a separate postoperative difficulty (Finlayson and Penfield 1941; Penfield 1958). It was a term used by Rasmussen as well. It consists of headache, stiff neck, and elevated body temperature. Its etiology was considered to be the result of blood in the cerebral ventricle, and it was felt that “ventricular closure” decreased its likelihood. The CSF examination at the time was amber in color and exhibited a leukocytosis, which was lower than what might have been expected with meningitis. Similar to Sect. 13.2.1, the term doesn’t really have the criteria to consider it a complication.

It is well known that mechanical retraction of cerebral cortex can transiently abolish whatever physiological function is associated with the retracted tissue. It has also been well known that excessive retraction, lasting for significant periods of time may not only transiently alter its function, but indeed may lead to permanent loss of function or even visually obvious destruction (bruising) of cortical tissue. Albin, a neuroanesthesiologist, and his colleagues conducted a number of studies on both human patients and experimental animals and demonstrated that pressures of greater than 30 mmHg applied to the brains of dogs for 60 min led to reductions in the somatosensory evoked potentials (SSEPs), even distant to the cortex that was actually being compressed (Albin et al. 1977, 1980; Albin and Bunegin 2003; Bennett et al. 1977a, b). Pressures that become “excessive” were those greater than 30 mmHg for these lengths of time—excessive in that they led to neurological deficits that lasted longer than 3 days and permanent histological neuronal loss in the compressed cortex. These effects were exaggerated if the cerebral blood flow to the animals was reduced significantly. RosenØrn and Diemer carried out similar studies with similar conclusions on rats (1982). Therefore, as mentioned earlier (Sects. 2.​2.​4 and 8.​4.​1), any retraction that is forceful should be applied to parenchyma that is being removed, not to that which is being left. (The surgery of an fHSPY is the only instance, in my view, in which traction may be applied to parenchyma that is being left, without much concern.)

This complication really needs no specific discussion here. It is obvious that arterial irrigation to cerebral parenchyma that is not being resected should be left healthy and most certainly with its blood supply intact. Any loss of this irrigation results in the loss or alteration of normal function, and if it is “eloquent” cortex, the loss of function will be associated with a postoperative neurological impairment. This begs a reiteration of the importance of recognizing the role of en passage arteries once again and the necessity of their preservation (Sect. 5.​2). If it involves the non-eloquent cortex, it may lead to the origin of epileptogenic foci, as Penfield warned in 1958.

Postoperative hemorrhage is not as common a clinical problem in epilepsy surgery as it is in general neurosurgery. If the epileptic surgery is truly resective, then there is space for minor hemorrhage to occur which is of little clinical significance. For example, the majority of resective epileptic surgery leaves behind a significant “empty space”—a space into which small self-limited postoperative hemorrhages may occur without any clinical evidence of such. On the other hand, that same hemorrhage in many general neurosurgical operations where there is no resection may well give rise to clinical symptomatology—symptomatology that may even be sufficiently significant to require a second operative procedure to remove the hemorrhage.

I noted the foregoing, not only for indicating the relatively minor postoperative hemorrhages that may be considered benign but also to follow up to indicate the clinical difference that may occur in the case of postoperative hemorrhages that are not self-limited. I have always remembered a patient who had a perfectly normal postoperative course for 36–48 h after a routine uneventful aTLY, who, in the period between the second and third postoperative days, began to exhibit a little bit of intermittent drowsiness, then some intermittent confusion, and finally some contralateral paresis. My initial thought was that this was simply more-than-usual edema; however, a CT clearly disclosed a temporal lobe resection cavity filled with blood and a midline displaced by a few millimeters. Thus, on the fourth day postoperative, the patient had her second operation! I mention this case, because we were taught, and we teach, that postoperative hemorrhage is usually found in the very early postoperative course, e.g., hours, or a day or so, following the completion of surgery. This is true, but in the case of significant resections, it is not only more likely to occur further (later) into the postoperative course, but also there is a rather more slowly developing clinical evidence of its presence. To summarize, the clinical evidence of a developing hemorrhage following significantly sized epileptic surgical resections is much more likely to be less acute than in operations that are unassociated with resections of cerebral parenchyma.