Classification of Seizures. Why do we need to classify seizures?. Different seizures affect different parts of the brain Different antiepileptic drugs are more effective with different seizures. Classification of Seizures. Partial Seizures - Simple partial - Complex partial
- Simple partial
- Complex partial
- Partial Seizures with Secondary Generalization
- Absence Seizures (Petit Mal)
- Atypical Absence Seizures
- Generalized, Tonic-Clonic Seizures (Grand Mal)
- Atonic Seizures
- Myoclonic Seizures
the seizure is a simple partial seizure
the seizure is a complex partial seizure
- déjà vu, flashbacks
- somatic sensation (paresthesias)
- vision (flashing lights or formed hallucinations)
- equilibrium (sensation of falling or vertigo)
- autonomic function (flushing, sweating, piloerection)
Partial Seizures with Secondary Generalization
Absence Seizures (Petit Mal)
Atypical Absence Seizures
Generalized, Tonic-Clonic Seizures (Grand Mal)
throughout the body
relaxation on the tonic muscle contraction
in the oral cavity, and the patient becomes
Generalized, Tonic-Clonic Seizures (Grand Mal)
Begins from a discrete region of the cortex which slowly spread to the neighbouring regions.
Divided into two phases:
Consists of 2 concurrent events occurring in an aggregate of neurons:
relatively long-lasting depolarization of neuronal membrane, initially initiated by the influx of Ca2+ from the ECF which later cause the opening of voltage-dependent Na+ channels and Na+ influx. This results in generation of repetitive AP. Depending on cell type, either GABA or K+ channels will cause hyperpolarization.
Synchronized burst from sufficient number of neurons will produce spike discharges seen on the ECG.
Spread of bursting activity normally prevented by 2 mechanism:
When sufficient neurons are recruited loss of surrounding inhibition propagation of seizure activity into:
Can be affected by various factors:
Conductance of ion channels, response characteristics of membrane receptors, cytoplasmic buffering, 2nd messenger systems and protein expression
Amount or type of neurotransmitters present at synapse, modulation of receptors by ECF ions and temporal and spatial properties of synaptic and non-synaptic input
Analogue of glutamate ( main excitatory NT in brain)
Antagonizes the effects of GABA at its recpetors reducing seizure threshold seizures!
Transformation of normal neuronal network into one which is chronically hyperexcitable.
Takes months to years between CNS injury and first seizure.
Pathologic studies of hippocampus of patients with TLE shows that:
Initial injury (very focal region) within the CNS
Recent identification of genetic mutations associated with variety of epilepsy syndromes important conceptual advances.
Found that many inherited idiopathic epilepsies are due to channelopathies (mutations affecting the ion channel fx.)
Current challenge is to identify multiple susceptibility genes that underlie the more common forms of idiopathic epilepsies.
Generally blocks the initiation and spread of seizures.
There are no ‘ anti-epileptogenic’ drugs available which helps prevent emergence of seizure formation following injuries
Presented with 3 episodes of seizures 1 day before admission.
3 epsiodes of seizure 1 day before admission
2 hr interval between episodes
Each episode lasts 20 seconds
No aura or premonition before the attacks
1st episode was while daughter was massaging
First seizure 17 y.o. within the CNS
Married at the age of 16 y.o.
1st episode before the birth of her first child.
Previously 1 / year
Lately more frequent
Usually > 1 fit per episode
She had 3 episodes of seizures in 2008.
On anti-epileptic drugs (?) from onset within the CNS
She took them regularly
Stopped 4 years ago as the doctor was worried about side effects
Frequency of attacks have increased
Weight loss from 86kg to 63kg in past 4 years
Currently complains of loss of sleep and loss of appetite
Newly diagnosed diabetic. Diagnosed on admission within the CNS
Glucose level = 9.5 mmol/L
Also a pre-hypertensive
Has leg swelling and slow healing leg ulcers since 3 yrs ago.
Father – Deceased. Had Type 2 DM and cardiovascular disease.
Mother – Deceased. Intestinal cancer.
Grandmother – 89 years old. Asthmatic
Father and uncle had epilepsy.
Married and has 4 children. All are healthy. None has epilepsy.
Works as a caterer.
Works hard and for long hours.
Believes work-related stress and tiredness may be the precipitating factor for her seizure attacks.
General : Patient was conscious, alert and communicative. She was lying supine on bed. She was in no obvious, respiratory distress, no obvious pain, no gadgets attached
Hands: No clubbing, no peripheral cyanosis, no delayed capillary refill, no koilonychia, no leukonychia, no splinter haemorrhages, no Janeway nodes or Osler’s lesions, no thenar and hypothenar muscle wasting
Blood pressure- 125/80 mmHg,
Heart rate- 72 beats permin
Respiratory rate- 15 breaths permin
Arms: No scratch matchs, no purpura, no ecchymosis, no bruises,no muscle wasting
Eyes: No jaundice, no pallor, no xanthelasma, no corneal archus
Mouth: Good oral hygiene, no leukoplakia, no angular stomatitis, no central cyanosis, Lips swollen due to biting during seizure episode.
Neck: No obvious swelling, no sinus discharge, JVP- 3cm, normal
Cardiovascular: Size and shape of chest is normal. No scars, no visible pulsation.
Upon palpation, apex beat cannot be located, no parasternal or apex heave, no palpable thrills.
Upon auscultation: Heart sounds rapid. Normal S1S2 sounds were heard, no murmurs, no additional sounds
Respiratory: No tracheal deviation, equal chest expansion on both sides, equal vibration on both sides, equal resonance on both sides, normal vesicular breath sounds heard, no bronchial or additional breath sounds,
Gastrointestinal: Not remarkable
Musculoskeletal: No obvious muscle wasting.Restricted movement of the right leg due to pain. Left leg normal.
Inspection: Not remarkable
Palpation: Not remarkable
- All reflexes are normal
Epileptic seizure secondary to hyperglycaemia
-Alcoholic or benzodiazepine withdrawal
-Psychoactive drugs (e.g., hallucinogens, cocaine)
Plasma Calcium levels (2.61 mmol/l)
High plasma glucose level. (24.6 mmol/l)
Fasting glucose level was 9.5 mmol/l
Has high cholesterol level (6.49 mmol/l)
High LDL levels (5.0 mmol/L)
Liver function tests and her renal function tests were normal
Her random blood glucose was monitored
she is put on a diabetic diet.
Patient Initials: TS
Registration Number: HTJ 403161
Age: 30 years old
Date of admission: 22nd April
Date of Clerking: 22nd April
Admitted to hospital for an episode of generalized tonic-clonic seizures
Admitted to hospital at 3.15 am for generalized tonic-clonic seizures. Seizures lasted for 2 minutes.
Jerking of upper and lower limbs and drooling of saliva during attack.
No urinary or fecal incontinence
Patient was sleeping during attack.
Seizures believed to have been brought upon by stress and headache.
Had headache the previous evening
First attack since February of 2008. within the CNS
h/o of MVA in 1997
First episode shortly after MVA
Diagnosed with epilepsy by doctor in Sungai Buloh.
h/o of multiple admission for seizures.
>2 episodes per year
Previously on meds (white pill with white line???). Stopped 2 years ago.
No fever. within the CNS
SOB x 2/7
Cough- productive yellowish sputum
MVA in 1997
Admitted to Sungai Buloh hospital and then transferred to GHKL
Coma for 3 weeks
No fractures. No neurosurgery done
Spent a further 2 weeks in the wards
Had first seizure attack shortly after discharge
Between 1997 and 2007, pt had around 15 seizures
Stopped meds 2yrs ago
Allergic to med (pink coloured tablet???) – develop rashes within the CNS
No known allergy to food
4th of 8 siblings.
No hx of epilepsy
No family hx of DM, HPT, asthma.
Mother: Deceased, cancer
Father: Deceased. Was an alcoholic
Younger brother: Deceased due to dengue
Works in a motor workshop
Smokes around 20 sticks of cigarette per day but has reduced to 10 per day. Smoking since 19 years old.
Social alcohol drinker. Stopped drinking 3 years ago.
BP: 107/71 mmHg
Pulse rate: 61 beats/min
Cranial Nerve examination: All normal
No loss of limb sensations
No upper limb weakness.
Lower limb weakness due to Phenytoin
On/off cramps of both legs
No diplopia. within the CNS
Babinski reflex: Negative
Lungs: Clear within the CNS
CVS: S1/S2 heard. No additional heart sounds.
P/A: Soft, non-tender, not distended
Plasma Fasting Blood Sugar – 4.5 mmol/L within the CNS
- pM cell < 25
- pM organisms (gram +ve cocci +++)
pM organisms (gram –ve bacilli +)
Coagulation Profile: within the CNS
- Prothrombin time : 13.0s
- INR : 1.08 (low) [2.0 – 2.5]
- aPTT : 34.7 s
Thyroid Function Test
- Plasma free T4 : 17.5 pmol/L
- Plasma TSH : 0.92 mU/L
Vitamin B12 – 307 pmol/L
EEG done in seven years ago after the first episode. within the CNS
No abnormalities found.
Patient’s Initials: SD
Age: 1 year old
Registration Number: HTJ 401311
Date of Admission: 16th April 2009
Date of Clerking: 17th April 2009
Present with fever, rhinitis and convulsions on the day of admission
Fever and rhinitis in the morning on the day of admission.
Relieved by anti-pyretic syrup
Convulsions in the evening.
Lasted only 5 minutes
Jerky movements of arms and legs. within the CNS
Rolling up of eyeballs
Drooling of saliva
No fecal or urinary incontinence
No poor feeding, vomiting, irritability, lethargy, drowsiness, loss of consciousness
No nausea/vomiting within the CNS
No sore throat
Temperature – 38.5⁰C
No hospitalization / surgery
No previous episode of epilepsy
BW 2.9kg, full term baby.
Spontaneous vaginal delivery
Follows immunisation programme
Last immunisation was for OPV, HiB, DPT, Hepatitis B. Due for MMR vaccination this year.
-No significant systemic findings
Brudzinski’s sign-flexion of the neck with the child supine causes flexion of the knees and hips
Kernig’s sign-with the child lying supine and with the hips and knees flexed, there is back pain on extension of the knee
Febrile convulsions secondary to upper respiratory tract infection.
Generalized Tonic Clonic
Don’t do anything!
Remove any objects around the area that might hurt the patient
Administer diazepam if available within the CNS
Call ambulance if seizure is more than 5 minutes, multiple episode within a short time and if the patient is hurt
No Seizures, No Side Effects
Discontinuation of therapy within the CNS
Should be considered only if seizure free more than 3 years
Slowly tapered down
If recur, resume previous drug dosages
Most patients can achieve complete control of seizures.
Most people lead a normal
Side Effects of drug therapy
Discourage risky activities
Avoid precipitating factors eg. Alcohol, fatigue etc
First aid measures
Racing heart within the CNS
Sudden loss of visionPresenting Complaint
CHILDREN,TEENAGERS within the CNS
DRIVING within the CNS
EMPLOYMENT within the CNS
RELATIONSHIP & MARRIAGE within the CNS
BRINGING UP CHILDREN within the CNS
OTHERS within the CNS
These are characterized by the site of the abnormal activity, e.g. pure sensory, motor, or psychic phenomena. But are associated with an impairment of consciousness
Complex partial seizures
These begin with features of simple or complex seizures, which then become generalized with tonic-clonic episodes. The initial partial element may be so shortlived that it may be only evident on the EEG.
Secondary generalized seizures
Usual onset in childhood. Characterized by loss of consciousness but maintained posture (stops talking an stares into space for seconds), blinking or rolling up of eyes with other repetitive motor actions. No post-ictal phase.
Adolescence onset. Involuntary jerking, particularly in the morning. They are associated with impairment of consciousness.
These are characterized by the site of the abnormal activity, e.g. pure sensory, motor, or psychic phenomena. They are not associated with impairment of consciousness.
Simple partial seizures
Vague symptoms before an attack (e.g dizziness, irritability), loss of consciousness. Tonic phase characterized by repetitive jerks, faecal or urinary incontinence, tongue biting. After a seizure, there is often impaired consciousness, lethargy, confusion, headache, back pain and stiffness.
Tonic-clonic (grand mal) seizures
A 20 y.o female student presents in the neurology outpatient department with a three-month history of ‘funny turns’ lasting 2-3 minutes. Each is preceded by an ‘odd sensation’, and is followed by a feeling of ‘vacancy’. She has no recollection of these events, but has been told about them by her friends, who say she becomes vacant and unresponsive, with grinding of her teeth and contortion of her face.
Epilepsy- absence seizure
RP, LFT, glucose level
Blood level of Calcium, Phosphate, Magnesium
Serum & urine alcohol and toxin screens
Blood levels of medication
Imaging: CT brain
Lumbar puncture (if CT shows no increased ICP)
List at least 4 therapeutic agents that may be used in this case, giving a side effect of each