CHAPTER 15
Electrical Activity of the Brain, Sleep–Wake States, & Circadian Rhythms 233Partial seizures originate in a small group of neurons and
can result from head injury, brain infection, stroke, or tumor,
but often the cause is unknown. Symptoms depend on the sei-
zure focus. They are further subdivided into
simple partial
seizures
(without loss of consciousness) and
complex partial
seizures
(with altered consciousness). An example of a partial
seizure is localized jerking movements in one hand progress-
ing to clonic movements of the entire arm.
Auras
typically
precede the onset of a partial seizure and include abnormal
sensations. The time after the seizure until normal neurologi-
cal function returns is called the
postictal period.
Generalized seizures are associated with widespread elec-
trical activity and involve both hemispheres simultaneously
.
They are further subdivided into
convulsive
and
nonconvul-
sive
categories depending on whether tonic or clonic move-
ments occur.
Absence seizures
(formerly called petit mal
seizures) are one of the forms of nonconvulsive generalized
seizures characterized by a momentary loss of consciousness.
They are associated with 3/s doublets, each consisting of a
typical spike and rounded wave, and lasting about 10 s (Fig-
ure 15–5). They are not accompanied by auras or postictal
periods.
The most common convulsive generalized seizure is
tonic–
clonic seizure
(formerly called grand mal seizure). This is
associated with sudden onset of contraction of limb muscles
(tonic phase)
lasting about 30 s, followed by a clonic phase
with symmetric jerking of the limbs as a result of alternating
contraction and relaxation
(clonic phase)
lasting 1–2 min.
There is fast EEG activity during the tonic phase. Slow waves,
each preceded by a spike, occur at the time of each clonic jerk.
For a while after the attack, slow waves are present.
Recent research provides insight into a possible role of
release of glutamate from astrocytes in the pathophysiology of
epilepsy. Also, there is evidence to support the view that reor-
ganization of astrocytes
along with dendritic sprouting and
new synapse formation form the structural basis for recurrent
excitation in the epileptic
brain. Clinical Box 15–1 describes
information regarding the role of genetic mutations in some
forms of epilepsy.
SLEEP–WAKE CYCLE
ALPHA, BETA, & GAMMA RHYTHMS
In adult humans who are awake but at rest with the mind wan-
dering and the eyes closed, the most prominent component of
the EEG is a fairly regular pattern of waves at a frequency of 8–
13 Hz and amplitude of 50–100
μ
V when recorded from the
scalp. This pattern is the
alpha rhythm
(Figure 15–6)
.
It is most
marked in the parietal and occipital lobes and is associated with
decreased levels of attention. A similar rhythm has been ob-
served in a wide variety of mammalian species. There are some
minor variations from species to species, but in all mammals the
pattern is remarkably similar (see Clinical Box 15–2).
When attention is focused on something, the alpha rhythm
is replaced by an irregular 13–30 Hz low-voltage activity, the
beta rhythm
(Figure 15–6). This phenomenon is called
alpha
block
and can be produced by any form of sensory stimula-
tion or mental concentration, such as solving arithmetic prob-
lems. Another term for this phenomenon is the
arousal
or
alerting response,
because it is correlated with the aroused,
alert state. It has also been called
desynchronization,
because
it represents breaking up of the obviously synchronized neuralFIGURE 15–5
Absence seizures.
Record of four cortical EEG
leads from a 6-year-old boy who, during the recording, had one of his
“blank spells” in which he was transiently unaware of his surroundings
and blinked his eyelids. Time is indicated by the horizontal calibration
line.
(Reproduced with permission from Waxman SG:
Neuroanatomy with Clinical
Correlations,
25th ed. McGraw-Hill, 2003.)
1 sCLINICAL BOX 15–1
Genetic Mutations & Epilepsy
Epilepsy has no geographical, racial, gender, or social bias.
It can occur at any age, but is most often diagnosed in in-
fancy, childhood, adolescence, and old age. According to
the World Health Organization, it is estimated that 50 mil-
lion people worldwide (8.2 per 1000 individuals) experi-
ence epileptic seizures. The prevalence in developing
countries (such as Colombia, Ecuador, India, Liberia, Nige-
ria, Panama, United Republic of Tanzania, and Venezuela) is
more than 10 per 1000. Many affected individuals experi-
ence unprovoked seizures, for no apparent reason, and
without any other neurological abnormalities. These are
called
idiopathic epilepsies
and are assumed to be ge-
netic in origin. Mutations in voltage-gated potassium, so-
dium, and chloride channels have been linked to some
forms of idiopathic epilepsy. Mutated ion channels can lead
to neuronal hyperexcitability via various pathogenic mech-
anisms. Scientists have recently identified the mutated
gene responsible for development of
childhood absence
epilepsy (CAE).
Several patients with CAE were found to
have mutations in a subunit gene of the GABA receptor
called
GABRB3.
Also, SCN1A and SCN1B mutations have
been identified in an inherited form of epilepsy called
gen-
eralized epilepsy with febrile seizures.
SCN1A and
SCN1B are sodium channel subunit genes that are widely
expressed within the nervous system. SCN1A mutations are
suspected in several forms of epilepsy.