Primary G.
S from the onset
PARTIAL EPILEPTIC
Motor, sensory, autonomic, or psychic
symptoms.
Without an obvious alteration in
consciousness. (Three additional features,)
1. Jacksonian march abnormal motor
movements may begin in a very restricted
region, and gradually progress (over seconds
to minutes).
2. May experience a localized paresis
(todd`s paralysis) minutes to many
hours.
3. Seizure may continue for hours or
days. epilepsia partials continua.
Other forms of simple-partial seizures include
those that cause changes in somatic
sensation.
Some patients describe odd internal feelings.
(fear, dej vu)
When precede a complex-partial or
secondarly generalized seizure, these simple
COMPLEX PARTIAL
SEIZURES
Focal seizure activity
Patient is unable to respond to visual or verbal
commands during the seizure and has
impaired recollection or awareness of the ictal
phase.[altered consciousness not loss of
cosnciousness as in generalised seizures]
Frequently begin with an aura.
The start of the ictal phase is often a sudden
behaivoral arrest or motionless stare.
Usually acompained by automatisms.
The patient is typically confused following the
seizure.(seconds up to an hour).
PARTIAL SEIZURES INTO
GENERALIZED SEIZURES
Partial seizures can spread to involve both
cerebral hemispheres and produce a
generalized seizur, usually of the tonic-clonic
variety
Is often difficult to distinguish from a primarilly
generalized tonic-clonic seizure.
Careful history identifies a preceding aura.
The Motor Cortex
-Paralysis of contralateral
GENERALIZED Secondary G. S from partial
SEIZURES becomes generalised
Absence seizures (Petit mal)
Sudden brief lapses of consciousness without loss of
postural control.
Typically last for only seconds, consiousness returns as
suddenly as it was lost.
No postictal confusion
Can occur hundreds of times per day.
Always begin in childhood (ages 4 to 8) or early
adolescence.
Generalised Tonic Clonic
Seizures
The most common seizure type resulting from metabolic
derangements.
The initial phase of the seizure is usually tonic contraction of
muscles throughout the body.
After 10 to 20 s. The tonic phase of the seizure typically
evolves into the clonic phase, produced by the
superimposition of periods of muscle relaxion on the tonic
muscle contraction.
The periods of relaxation progressively increase until the
end of the ictal phase.
Usually last no more than 1 min.
Status epilepticus
epilepticus more than 20 years ago as a single epileptic
seizure of >30 minutes duration or a series of epileptic
seizures during which function is not regained between ictal
events in a 30 minute period
Because of the clinical urgency in treating generalized
convulsive status epilepticus (GCSE), Once seizures have
continued for more than a few minutes, treatment should
begin.
Considering the need for rapid evaluation and intervention
in GCSE, an accepted operational definition of status
Atonic seizures
Sudden loss of postural muscle tone lasting 1 to 2 s.
Consciousness is briefly impaired
Usually no postictal confusion
Very brief seizure may cause only a quick head drop or nodding
movement.
Longer seizure will cause the patient to collapse. (extremelly
Myoclonic seizures
The Frontal Eye Lid The Motor Speech Area of
-Lesion of frontal eye field of Broca
Sudden and brief muscle contraction that may involve one part of
the body or the entire body.
Pathologic myoclonus is most commonly seen in association with
metabolic disorders, degenerative CNS diseases, or anoxic brain
injury.
extremities + finer & more
skilled movements suffering
most
Produce more damage than
destruction of secondary area
-Destruction of both areas
produce complete contralateral
paralysis
-Jacksonian epileptic seizure ->
irritative lesion of primary
motor area
The Sensory Speech Area of
Wernicke
-Lesion restricted to Wernicke
speech area in the dominant
hemisphere produce of ability
to understand spoken and
written word called receptive
aphasia
-Since Broca area unaffected,
speech is unimpaired & pt can
produce fluent speech but pt is
unaware of meaning of words
pt uses//using nonexistence
words + pt not aware of any
mistakes
The Prefrontal Cortex
-Destruction of prefrontal
region does not produce
marked loss of intelligence
-PC necessary for production of
abstract ideas, judgement,
emotional feeling & personality
-Tumor/trauma in PC -> person
losing initiative & judgement
-Emotion changes can cause
euphoria, change social
behaviour, careless of dress+
appearance
The Sensory Cortex
-Thalamus relays a large part
of sensory signals to cerebral
cortex for analysis
-SC is necessary for
appreciation of spatial
recognition, relative intensity &
recognition of similarities & diff
- Lesion on primary
somesthetic area->
contralateral sensory
disturbances and most severe
in distal parts of limbs.
-Pt unable to judge degree of
warmth, localize tactus stimuli
accurately & unable to judge
weight of object
one hemisphere -> 2 eyes to
deviate to side of lesion &
inability to turn eye to opposite
side
-Tracking movement of eyes
when following moving objects
is unaffected because lesion
does not incolve the visual
cortex in the occipital lobe
The Motor and Sensory Speech
Areas
-Destructive lesion in Broca
and Wrnicke -> loss of speech
production & understanding
spoken & written word called
global aphasia
-Pt having lesion along insula
have difficulty pronouncing
phonemes in their proper order
& produces sound that are
close to the target word but
not exactly correct.
The PC & Schizophrenia
-PC is rich in dopaminergic
innvervation
-Failure of innervations->
symptoms of schizophrenia
include disorder of tought
-Blood flow in PC of
Schizophrenia is reduced
The Somesthetic Area
-Lesion of sup parietal lobe
interfere with pts ability to
touch, pressure &
proprioceptive impulses-> to
appreciate texture, size, form
-Asterogenesis-> Loss of
integration of sensory impulses
-Lesion of post parietal lobe ->
interfere with appreciation of
body image on opposite side of
the body
-Individual fail to recognize
opposite side of the body
(cannot wash, shave, dress the
opposite side)
-Lesion in left frontal gyrus->
loss of ability to produce
speech called expressive
aphasia
-Pt retain ability to think the
words they wish to say, they
can write the words & can
understand their meaning
when they see or hear
The Dominant Angular Gyrus
-Lesion in the angular gyrus in
post parietal lobe divide the
pathway between the visul
association area & the ant part
of Wernicke area causing pt
unable to read (alexia) // write
(agraphia)
Frontal Leukotomy and Frontal
Lobectomy
-to emotional responsiveness
of pts with emotional
responsiveness of pts with
emotional obsession &
intractable pain
-removal will cause the past
experience & possibilities of
future is not recalled->
introspection
-Pt suffering severe pain will
still feel pain after lobectomy
but the person will not worry
about the pain-> will not suffer
The Primary Visual Area
-Lesion on post part of calcirine
sulcus-> loss of sight in the
opposite visual field, crossed
homonymous hemianopia
- Loss of muscle tone->
symptoms of SC lesion
The Secondary Visual Area
-Lesion results in a loss of
ability to recognize objects
seen in opposite field of vision-
> area of cortex that stores
past visual experience has
been lost
The Primary Auditory Area
-PAA in inf wall of lat sulcus
receives nerve fibres from both
cochlea-> lesion in one cortical
area produce bilateral loss of
hearing
-Loss of ability to locate the
source of sound-> MAIN
DEFECT
-BILATERAL DESTRUCTION of
primary auditory area->
complete deafness
The Secondary Auditory Area
-Lesion of cortex post to
primary auditory area in lateral
sulcus and sup part of
temporal lobe-> inability to
interpret sounds
-Pt suffering from WORD
DEAFNESS//ACOUSTIC VERBAL
AGNOSIA
Neurotransmission signaling pathway

Glutamate and -aminobutyric acid (GABA) are the two neurotransmitters related
to epilepsy.

Glutamate and -aminobutyric acid (GABA) are the two neurotransmitters that
have been studied extensively in relation to epilepsy.

Glutamate is a main excitatory neurotrans-mitter in brain that is responsible for

generating excitatory postsynaptic potentials by depolarizing the neurons

glutamate receptors are classified into ionotropic receptors: (AMPA), (NMDA)

and kainate, and metabotropic (G protein-coupled) receptors

upregulation of glutamate receptors, elevation in extra-cellular glutamate

concentration, abnormalities in glutamatergic transporters, autoimmune
mechanism -> initiation and progression of epilepsy-> contribute to excessive
glutamatergic activity-> important role in hyperexcitability and epilepsy->
recorded as an interictal spike on electroencephalogram, known as paroxysmal
depolarizing shift is intracellularly associated with epileptic discharges in
neurons-> due to a giant excitatory synaptic potential with characteristic of burst
discharge, which is dependent on activation of AMPA receptors & NMDA
receptors

GABA is recognized as the main inhibitory neurotransmitter-> generates

inhibitory presynaptic potentials by hyperpolarizing the neurons

GABAergic system-> counter-balancing the neuronal excitation + suppressing

the epileptiform discharges

Two types of GABA receptors that are involved in pathogenesis of epilepsy,

namely GABAA and GABAB receptors. GABAA receptors-> mediate rapid inhibitory
presynaptic potentials by increasing influx of chloride. GABA B receptors->
mediate slow inhibitory presynaptic potentials by increasing the potassium
conductance and decreasing the calcium entry

reduction or loss of GABAergic inhibition may increase the probability of

generating excitatory postsynaptic potentials and synchronizing burst
discharges, and therefore induce epileptogenesis \

Molecular and genetic mechanisms: Ion channels and receptors

Channelopathy-> ion channel dysfunction or defect

Ion channels are pore-forming proteins along the lipid membrane of cells that
allow movement of selected ions across cell membranes to maintain negative
resting membrane potential inside the cells. voltage-gated channels controlled
by changes in membrane potential and ligand-gated channels that are activated
by ligand binding such as GABA and acetylcholine neurotransmitters