Alcohol and seizures(Seizures – Medical Causes and management)

Dr Pratyush Chaudhuri

Introduction

• Alcohol abuse is the commonest cause of adult onset seizures.

• 82% of trauma and about 73% of adult onset seizure in my practice.

• Terminology: Alcohol Related Seizure (ARS)

History

• First recorded by Hippocrates 400BC

• 1852- Huss described – Rum fits

• Victor & Adams – first systemic study and clinical data publication about withdrawal syndromes.

Pathogenesis of seizure related to drinking alcohol

• Complex biochemical mechanism.• Alcohol is a general anaesthetic with anti-convulsant

properties.

• Causes change in membrane properties and may be responsible for alteration in membrane receptors.

• Alcohol specifically potentiates the post synaptic effect of γ-aminobuteric acid (GABA).

• Modulation of G proteins

• Modulation of calcium channel

Differential diagnosis

Differential diagnosis of seizures in alcohol dependant patient.

1. Withdrawal from alcohol

2. Withdrawal from drugs (benzodiazapines, barbiturates and narcotics)

3. Exacerbation of idiopathic or post traumatic epilepsy

4. Acute overdose(alcohol, amphetamine , cocain, anticholinergics, phenothiazines, tricyclics and isoniazide)

5. Metabolic disorders ( Hypoglycemia, hyponatremia, hypomagnesemia & hypocalcemia)

6. CNS disorder Acute head trauma, infection (meningitis, encephalitis and brain abscess), stroke

7. Noncompliance with anticonvulsant medication

Partial or complete withdrawal of alcohol

• Major cause • GTC type • About 7 – 48 hrs after cessation of alcohol

consumption.

• Possibly by alteration GABA receptor sensitivity

Alcohol as central nervous system toxin.

1. Direct epileptogenic effect.

2. Risk is higher for non drinker consuming > 12g alcohol.

Supported by the finding that hemodialysis helps alcoholic patients with seizures.

Metabolic disorder

• Alkalosis: hyperventilation with resultant respiratory alkalosis

Hyper-excitability of the CNS

Lowering of seizure threshold ( possible due to lowering of ionised sr calcium)

• Hypo-Magnesemia: suggested as a cause.

• No strong evidence

• Studies failed to show measurable low magnesium in blood.

Hypoglycemia• Several factors contribute1. Depletion of liver glycogen2. Decreased nutrition support3. Decreased cortisol level4. Sepsis and hypothermia.

• Systematic studies – no correlation (lacking significant corelation between the blood sugar level and seizures)

Acute intoxication or poisoning1. Ingestion of other drugs – may ppt a seizure.2. Medication for co-morbid disease like INH,

antidepressant (tricyclics) and anti-psychotics (phenothiazines)

3. Withdrawal from GABA receptor analogues4. Other drugs

Pre-existing epilepsy

1. Stimulant effect (systematic data prove that this is least likely)

2. Withdrawal phenomenon3. Non-compliance to anti-convulsant4. Alteration of absorption of drug5. Enhancement of anti-epiletic drug metabolism

• Structural abnormality1. Increased incidence of CVA, hemorrhagic stroke and SAH.2. Alcohol causes cerebral vaso-spasm3. Micro infarction due to increased platelet and erythrocyte

aggregation.4. Change in coagulation and platelet aggregation.5. Head trauma6. Cerebral atrophy

management

• Objectives

1. Treatment of convulsions and associated symptoms of withdrawal

2. Identification and treatment of coexisting structural and/or toxic-metabolic causes of seizure.

Initial assessment• ABC• IV access and primary management as done for most patients

of epilepsy• Check blood sugar level• Get information about what medicines is the patient

presently taking.• 12 lead ECG – identify intra-ventricular conduction delays and

heart block- primary emergency. • Patient should receive 100mg thiamine along with dextrose

infusion + 2 gm of magnesium sulphate.

• Laboratory• Routine physician profile• Toxin profile if suspected (alcohol amphetamine, cocaine,

marijuana, phencyclidine)

• If on anticonvulsants- may consider doing drug levels.

• Diagnostic examination

• X Ray Chest & cervical spine.• CT scan brain • EEG

Management

• BenzodiazpinesLorazepam is the drug of choice:

Because of • Minimal depressant action on respiration and circulation• Shorter half life• No active metabolites • Prolonged period of action• Half life not affected by liver or renal dysfunction.

Barbiturates (phenobarbitone)• Good for control of seizures

• Narrow therapeutic index • Known to increase hepatic enzyme activity.

Anti-epileptic drugs

• Patients wit ARS without coexisting structural abnormalities or pre-existing epilepsy do not require anticonvulsant therapy.

• Patient with new onset seizure should be admitted to the hospital in the setting of chronic alcohol abuse

That’s it !