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. Direct epileptogenic effect. 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 contribute Depletion of liver glycogen Decreased nutrition support Decreased cortisol level Sepsis and hypothermia. Systematic studies  – no correlation  (lacking significant corelation between the blood sugar level and seizures)
Acute intoxication or poisoning Ingestion of other drugs – may ppt a seizure. Medication for co-morbid disease like INH, antidepressant (tricyclics) and anti-psychotics (phenothiazines) Withdrawal from GABA receptor analogues Other drugs
 
Pre-existing epilepsy Stimulant effect  (systematic data prove that this is least likely) Withdrawal phenomenon Non-compliance to anti-convulsant Alteration of absorption of drug Enhancement of anti-epiletic drug metabolism
Structural abnormality Increased incidence of CVA, hemorrhagic stroke and SAH. Alcohol causes cerebral vaso-spasm Micro infarction due to increased platelet and erythrocyte aggregation. Change in coagulation and platelet aggregation. Head trauma Cerebral atrophy
management Objectives Treatment of convulsions and associated symptoms of withdrawal 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 Benzodiazpines Lorazepam 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 !

Alcohol and seizures

  • 1.
  • 2.
    Alcohol and seizures(Seizures – Medical Causes and management) Dr Pratyush Chaudhuri
  • 3.
  • 4.
    Introduction Alcohol abuseis 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)
  • 5.
    History First recordedby Hippocrates 400BC 1852- Huss described – Rum fits Victor & Adams – first systemic study and clinical data publication about withdrawal syndromes.
  • 6.
    Pathogenesis of seizurerelated 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.
  • 7.
  • 8.
    Alcohol specifically potentiatesthe post synaptic effect of γ -aminobuteric acid (GABA). Modulation of G proteins Modulation of calcium channel
  • 9.
    Differential diagnosis Differentialdiagnosis 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
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  • 11.
    Partial or completewithdrawal of alcohol Major cause GTC type About 7 – 48 hrs after cessation of alcohol consumption. Possibly by alteration GABA receptor sensitivity
  • 12.
    Alcohol as centralnervous system toxin. Direct epileptogenic effect. Risk is higher for non drinker consuming > 12g alcohol. Supported by the finding that hemodialysis helps alcoholic patients with seizures.
  • 13.
  • 14.
    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)
  • 15.
    Hypo-Magnesemia : suggestedas a cause. No strong evidence Studies failed to show measurable low magnesium in blood.
  • 16.
    Hypoglycemia Several factorscontribute Depletion of liver glycogen Decreased nutrition support Decreased cortisol level Sepsis and hypothermia. Systematic studies – no correlation (lacking significant corelation between the blood sugar level and seizures)
  • 17.
    Acute intoxication orpoisoning Ingestion of other drugs – may ppt a seizure. Medication for co-morbid disease like INH, antidepressant (tricyclics) and anti-psychotics (phenothiazines) Withdrawal from GABA receptor analogues Other drugs
  • 18.
  • 19.
    Pre-existing epilepsy Stimulanteffect (systematic data prove that this is least likely) Withdrawal phenomenon Non-compliance to anti-convulsant Alteration of absorption of drug Enhancement of anti-epiletic drug metabolism
  • 20.
    Structural abnormality Increasedincidence of CVA, hemorrhagic stroke and SAH. Alcohol causes cerebral vaso-spasm Micro infarction due to increased platelet and erythrocyte aggregation. Change in coagulation and platelet aggregation. Head trauma Cerebral atrophy
  • 21.
    management Objectives Treatmentof convulsions and associated symptoms of withdrawal Identification and treatment of coexisting structural and/or toxic-metabolic causes of seizure.
  • 22.
    Initial assessment ABCIV 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.
  • 23.
  • 24.
    Laboratory Routine physicianprofile Toxin profile if suspected (alcohol amphetamine, cocaine, marijuana, phencyclidine) If on anticonvulsants- may consider doing drug levels.
  • 25.
    Diagnostic examination XRay Chest & cervical spine. CT scan brain EEG
  • 26.
    Management Benzodiazpines Lorazepamis 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.
  • 27.
  • 28.
    Barbiturates (phenobarbitone) Goodfor control of seizures Narrow therapeutic index Known to increase hepatic enzyme activity.
  • 29.
    Anti-epileptic drugs Patientswit ARS without coexisting structural abnormalities or pre-existing epilepsy do not require anticonvulsant therapy.
  • 30.
    Patient with newonset seizure should be admitted to the hospital in the setting of chronic alcohol abuse
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