An update on psychopharmacology part i 22 june 2007 fountain house

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  • 1. AN UPDATE ON PSYCHOPHARMACOLOGY Prof. Dr. Haroon Rashid Chaudhry FACHARZT (Psych & Neurology) MRCPsych (London), FACP (USA), FAPA (USA), FRCP (Ireland)
    • Head Department of Psychiatry
    • FJMC & SGRH
    • Zonal Representative World Psychiatric Association (WPA)
    • Vice President World Federation for Mental Health (WFMH)
    • Honorary Executive Director
    • Fountain House, Lahore
    • President Elect Pakistan Psychiatric Society (PPS)
  • 2.
    • Anti-depressants
    • Mood stabilizers
    • Anti-anxiety drugs
    • Anti-psychotic drugs
    • Anti-epileptic drugs
    • Anti-dementia drugs
  • 3. ANTI-DEPRESSANTS
  • 4.
    • Imipramine (Kuhn 1957) 1 st TCA
    • Iproniazide (Loomer Saunders & Kline 1957) 1 st MAOA
    HISTORY
  • 5.
    • Serotonin
    • Norepinephrine
    • Imipramine
    • Amitryptiline
    • Clomipramine
    • Dothiepin
    • Nortriptyline
    NEUROTRANSMITTERS ADDRESSED TRICYCLIC ANTI- DEPRESSANTS (TCAS )
  • 6.
      • Time Tested
      • Established Efficacy
    • BUT HIGH RISK FOR
      • Cardiac Pts
      • Epileptic Pts
      • Glaucoma Pts
      • Patients with Enlarged Prostate
      • Overdose
    • ADDITIONAL RISK FOR
      • Cancer Pts
      • Hepatitis pts
      • Old Age
    TCAs
  • 7.
    • SIDE EFFECTS
    • Dryness of mouth
    • Constipation
    • Blurring
    • Urine Retention
    • Tachycardia
    • Postural Hypotension
    •  Conduction
    •  Contractility
    TCAs
  • 8.
    • Maprotiline
    • Mianserin
    SEARCH FOR SAFER ANTIDEPRESSANTS EFFICACY vs. SAFETY =± TCAs >TCAs
  • 9.
    • Irreversible MAOIs
      • Phenelzine
      • Tranylcypromine
    • Precautions
      • Dietary Restrictions
      • Serious Interactions
    MONOAMINE OXIDASE INHIBITORS (MAOIs )
  • 10.
    • IMPROVED SAFETY
      • Reversible MAOIs
      • Moclobamide
      • Befloxatone
    MAOIs
  • 11. SINGLE NEUROTRANSMITTER ADDRESSED SEROTONIN
  • 12.
    • Fluoxetine
    • Fluvoxamine
    • Paroxetine
    • Sertraline
    • Citalopram
    SELECTIVE SEROTONIN REUPTAKE INHIBITORS (SSRIs)
  • 13. SELECTIVE SEROTONIN REUPTAKE INHIBITORS (SSRIs)
    • Fluoxetine
    • Fluvoxamine
    • Citalopram
    • Sertraline
    • Paroxetine
    • Major Depression
    • Prophylaxis of Recurrent Major Depression
    • Treat. Of Secondary Depression e.g., Schizophrenia, Dementia
    • Bulimia
    • OCD
    • Phobic Disorder
    • Panic Disorder
    • Alcohol /Sub. Abuse
  • 14. SSRIs EFFICACY vs. SAFETY = TCAs >TCAs
  • 15.
    • Fluoxetine Weekly
    • Escitalopram
    • Paroxetine SR
    IMPROVED EFFICACY
  • 16. SINGLE RECEPTOR SELECTIVITY SEROTONIN-REUPTAKE INHIBITORS/ RECEPTOR BLOCKERS TRAZODONE NEFAZODONE
  • 17. EFFICACY vs SAFETY =TCAs >>TCAs
  • 18.
    • Readdressed
      • Norepinephrine
    • Reboxetine
    SINGLE NEUROTRANSMITTER
  • 19. SELECTIVE DOPAMINE REUPTAKE INHIBITORS (SDRIs)
    • BUPROPION
    • Major Depression
    • Prophylaxis of Recurrent Major Depression
    • Bipolar Depression
    • ADHD
    • Alcohol, Nicotine Dependence
  • 20.
    • Venlafaxine
    • Milancipran
    • Duloxetine
    DUAL ACTION READDRESSED SNRIs
    • Serotonin
    • Norepinephrine (Dopamine)
  • 21. EFFICACY vs SAFETY ( =/>?TCAs (>>TCAs)
  • 22.
    • Mirtazepine
    NASSA EFFICACY vs. SAFETY (=/> TCAs (>>>TCAs)
  • 23. MOOD STABLIZERS
  • 24. HOW SHOULD WE DEFINE A “MOOD STABILIZERS”?
    • No common definition exists today
    • Debate about key features
  • 25. MOOD STABILIZERS: POSSIBLE FEATURES
    • Acute antimanic effects
    • Prevention of manic episodes
    • Acute antidepressant effects in mixed patients
    • Prevention of depressive episodes
    • Prevention of rapid cycling
    • amelioration of residual symptoms
    • Do not precipitate manic episodes
    • Do not precipitate depressive episodes
  • 26. EFFECTIVENESS OF POSSIBLE MOOD STABLIZERS Acute Acute Acute Maint- Mania Mixed Rapid enance States Cyclers Lithium Yes No? No? Yes Valproate Yes Yes Yes Yes Carbamazepine (Yes) Yes Yes Yes Olanzapine/ Yes Yes Yes Pending* Clozapine * Open extension data positive for olanzapine
  • 27. VALPROATE: AD EFFICACY
    • Open study 1 (N=55)
      • Moderate to Marked Improvement = 47%
    • Open study 2  (N=103)
      • Moderate improvement = 22%
    • 1 calabrese JR, Delucchi GA, Am J Psychiatry. 1990; 147(4)431-434.
    • Lambert, 1984.
  • 28. PRECIPITATION OF MOOD EPISODES Mania Depression Lithium No No Valproate No No Carbamazepine No No Olanzapine/ No No Clozapine Antidepressants Yes No Typial antipsychotics No Probable
  • 29. EASE OF USE OF MOOD STABILIZERS Simple Frequent Lab Prescribing Monitoring Lithium No Yes Valproate Somewhat Somewhat Carbamazepine No Yes Olanzapine/ Yes No Clozapine No Yes
  • 30. SIDE EFFECTS OF MOOD STABILIZERS Lithium Weight gain, tremor, Gl symptoms,  thyroid function, cognitive complaints Valproate Weight gain, (  thyroid function), Gl upset, pancreatitis, ? Polycystic ovaries Carbamazepine  WBC, rashes, nausea Olanzapine/ Weight gain, sedation ? Hyperglycemia Clozapine Weight gain, sedation, agranulocytosis,  salivation, ? hyperglycemia
  • 31. OPTIMAL WORKING DEFINITION OF MOOD STABILIZER
    • Primary considerations
      • Effective in acute mania
      • Effective in acutely reducing depressive symptoms in mixed states
      • Prevents episodes of both mania and depression
      • Does not precipitate mania or depression
    • Secondary considerations
      • Efficacy in rapid cycling
      • Reduction of residual symptoms
  • 32. PUTATIVE/INNOVATIVE MOOD STABILIZERS FOR REFRACTORY BIPOLAR PATIENTS Anticonvulsants Ca2+Channel Blockers Gabapentin Verapamil Lamotrigine Nifedipine topiramate Nimodipine Tiagabine Acetazolamide
  • 33. Atypical Antipsychotics Hormonal Clozapine thyroxine Risperidone Estrogen/progesterone Olanzapine Tamoxifen Quetiapine (Ziprasidone) Other Tryptophan Choline Donepezil Omega-3 fatty acids PUTATIVE/INNOVATIVE MOOD STABILIZERS FOR REFRACTORY BIPOLAR PATIENTS
  • 34. MOOD STABILIZER: MANIA
    • Mania with psychosis: * Divalproex - * Lithium
    • (Olanzapine, Risperidone, High potency conventional)
    • Dysphoric mania: * Divalproex - * Lithium
    • Epuphoric mania: * Lithium - * Divalproex
    • Hypomania: * Lithium - * Divalproex
  • 35. MOOD STABILIZER: DEPRESSION
    • Without an AD: * Lithium * Divalproex
    • *Lamotrigine * Carbamazepine
    • With an AD: * Lithium - * Divalproex
    • * Lamotrigine * Caramazepine
    • With psychosis: * Olanzapine - * Risperidone
    • * Quetiapine * Conventional
  • 36. Lithium Divalproex Carbamazepine First Line Lamotrigine ? Gabapentin Olanzapine Topiramate Efficacy in Depression Clinical Features ?
  • 37. BIPOLAR DISORDERS: RELAPSE PREVENTION
    • Bipolar disorders are recurrent
      • Recurrence has clinical, medical, psychosocial, and economic effects.
      • Recurrence results in hospitalization
        • Mania or depression (Bipolar I)
        • Depression (Bipolar II)
    • Recurrence results in cycle shortening
  • 38. BIPOLAR RECURRENCE: CLINICAL EFFECTS
    •  Rate of substance abuse comorbidity
    •  Rate of alcoholism comorbidity
    •  Rate of suicide
    • Possible treatment refractoriness
  • 39. BIPOLAR RECURRENCE: MEDICAL EFFECTS
    •  Risk of cardiac disease
    •  Risk of drug interactions
  • 40. BIPOLAR RECURRENCE: PSYCHOSICAL EFFECTS
    •  Rates of divorce, separation
    •  Possibility of jail/prison or hospitalization
  • 41. BIPOLAR RECURRENCE: ECONOMIC EFFECTS
    •  Job performance
    •  Medical treatment costs
    •  Psychiatric treatment costs
  • 42. BIPOLAR DISORDERS: RELAPSE PREVENTION
    • Bipolar disorders are recurrent
      • Recurrence has clinical, medical, psychosocial, and economic effects.
      • Recurrence results in hospitalization
        • Mania or depression (Bipolar I)
        • Depression (Bipolar II)
    • Recurrence results in cycle shortening
  • 43. PREDICTORS OF POOR LONG-TERM RESPONSE WITH LITHIUM
    • Psychosis
    • Substance abuse
    • Rapid cycling
    • More than 3 episodes
    • Mixed mania (depression and mania)
    • Poor compliance
  • 44. PROBLEMS OF CURRENT MOOD STABILIZERS
    • Limited efficacy
    • Toxicity
    • Side effects: renal, thyroid, hematologic, hepatic
    • Monitoring
    • Interactions
    • Teratogenicity
    • Weight gain
    • Poor compliance
    • Refractoriness
  • 45. BIPOLAR DISORDERS: TREATMENTS THAT DECREASE RISK OF RECURRENCE
    • Lithium
    • Anticonvulsant mood stablizers (carbamazepine, divalproex, Lamotrigine)
    • Possibly benzodiazepines (clonazepam)
    • Possibly ECT
    • Possibly clozapine
  • 46.
    • Tricyclic antidepressants
    • “ Typical” neuroleptics
    • Gabapentin
    • Nonmood stablizing anticonvulsants
    • Alprazolam
    BIPOLAR DISORDERS: TREATMENTS THAT INCREASE RISK OF RECURRENCE
  • 47.
    • “ Atypical” neuroleptics
    • Risperidone
    • Olanzapine
    • Quetiapine
    • Ziprasidone
    BIPOLAR DISORDERS: Treatments Being Studied to Determine Risk of Recurrence
  • 48.
    • Improve illness awareness
    • Early identification of new episodes
    • Enhance compliance
    • Stress management
    • Avoid substance abuse
    GOALS OF PSYCHOEDUCATION IN BIPOLAR PATIENTS
  • 49.
    • Treat the illness, not just the episodes
    • Help the patient learn about destabilizing factors
    • Be empathetic, but blunt, about illness and denial
    • Work to achieve recovery, not limited improvement.
    • Use regimens that yield excellent tolerability and adherence
    • Acute episode drug needs are often different from maintenance, but they interact significantly
    PRINCIPLES OF BIPOLAR DISORDER
  • 50. Case Vignette
    • Ms. X is an attractive 21 year old final semester engineering student, an active member of her college literary and drama club presented with a 10 day history of excessive cheerfulness, over talkativeness, spending sprees, endless partying, insomnia, and suspicions of being teased and harmed.
    • She has no past history of medical/ mental illness/ no substance use.
    • Family history revealed an episodic illness in mother stabilized on lithium.
  • 51. Case Vignette
    • Psychiatric examination revealed
      • Increased PMA
      • Flight of ideas
      • Elated mood
      • Inflated self esteem
      • Delusions of persecution and reference
    • Detailed medical evaluation, investigations ruled out any organic / systemic dysfunction
  • 52. Case Vignette
    • A consultant Psychiatrist made a diagnosis of Mania with psychotic symptoms (ICD 10) [DSM IV TR Bipolar I disorder Single manic episode severe with psychotic features] and she was hospitalized.
  • 53.
    • What will be your drug regime
      • Mood stabilizers alone (LI/DVX)
      • Antipsychotics alone (AAP/TAP)
      • Mood stabilizers (Li/DVX) + Antipsychotics (AAP/TAP)
      • Mood stabilizers + Benzodiazepines
      • Mood stabilizers + Antipsychotics + Benzodiazepines
    MANIA WITH PSYCHOTIC SYMPTOMS
  • 54. Rapid cycling 10 – 20% Mixed (dysphoric) 30 – 50% Pure mania 30 – 50% VPA VPA Li, VPA Olanz, VPA ? GB BP II Dep Lamotrigine Not listed in DSM IV TR. Anxiety, Hostility, Impulsivity, Poor insight, Confusion, Memory impairment Sensory hyper acuity Mania with psychotic Features 25 – 75% Mood Stabilizer Combinations Phenomenological Domains
  • 55. ANTI-ANXIETY DRUGS
  • 56. a) BENZODIAZEPINES
    • Short Acting
    • Intermediate
    • Long Acting
    b) NON BENZODIAZEPINES
    • Buspirone
    • Etifoxine HCI
  • 57. BENZODIAZEPINES PROS / CONS
    • Established Efficacy
    • Safety in Over Dose
    • Withdrawal Effects
    • Dependence
    • Tolerance
    • Memory Disturbance
    • Rebound Anxiety
  • 58. BENZODIAZEPINES A FRIEND FOE ? OR
  • 59. History of Anxiolytic Development ALCOHOL 1903 - BARBITURATES 1950’s – NON BARBITURATES (Meprobamate) LATE 50’s - BENZODIAZEPINES NONBENZODIAZEPINE HYPNOTICS GABA MIMETICS SELECTIVE GABA A TARGETS
  • 60. SIX ISSUES
    • Do we have any neuropsychiatric disorders without contribution of the GABA-BZD receptor complex?
    • Wouldn’t a world without benzodiazepines make the patients anxious, the psychiatrists restless, the pharma industry insomniacs, and the society bewildered?
    • Don’t we think that the ‘GOOD’ that benzodiazepines have provided, are providing and will provide far outweigh the questionable ‘BAD’ about benzodiazepines?
  • 61.
    • 4. Do we have enough evidence on
      • BZD and cognitive dysfunction?
      • BZD and oversedation?
      • BZD and dependence potential?
      • BZD withdrawal?
    • 5. Are we aware of what we are talking about?
    • 6. Can we balance the options?
  • 62.
    • Do we have any neuropsychiatric disorders without contribution of the GABA-BZD receptor complex?
    ISSUE 1
  • 63.
    • Anxiety
      • Preclinical and clinical evidence is robust
      • BZD are effective anxiolytics
    • Depression
      • Behavioural models have shown depression in animal can be manipulated by GABA agents
      • Stress is key to depression and stress induced changes occur in GABAergic function
    GABA BZD IN NEUROPSYCHIATRY
  • 64.
    • Schizophrenia
      • Several lines of evidence support the role of an epigenetic-induced GABAergic cortical dysfunction
      • in schizophrenia psychopathology
    • Addiction
      • Decreased GABAergic function is a major etiologic step in the maintenance of addictive state
    GABA BZD IN NEUROPSYCHIATRY
  • 65.
    • Other disorders
      • Epilepsy
      • Catatonia
      • ADHD
      • PMDD
      • Dyskinesias/Akathisia
      • Tourettes
      • Parkinsons
      • Huntington’s disease
    GABA BZD IN NEUROPSYCHIATRY
  • 66.
    • Wouldn’t a world without benzodiazepines make the patients anxious, the psychiatrists restless, the pharma industry insomniacs, and the society bewildered?
    ISSUE 2
  • 67.
    • Benzodiazepines have often been called the most widely prescribed group of drugs in the world and the biggest selling drugs in the history of medicine.
    • Worldwide sales of benzodiazepines are estimated at in excess of $21 billion.
    • 1980’s 1 billion alprazolam prescription worldwide
    • Non psychiatric prescriptions account for 70% of benzodiazepine
      • Physicians
      • Cardiologists
      • Gastroenterologists etc
    BENZODIAZEPINE IN PRACTICE
  • 68.
    • Don’t we think that the ‘GOOD’ that benzodiazepines have provided, are providing and will provide far outweigh the questionable ‘BAD’ about benzodiazepines?
    ISSUE 3
  • 69.
    • Do we have enough evidence on
      • BZD and cognitive dysfunction?
      • BZD and oversedation?
      • BZD and dependence potential?
      • BZD withdrawal?
    ISSUE 4
  • 70.
    • Cognitive effects of long-term benzodiazepine use: a meta-analysis
    • Moderate-to-large weighted effect sizes were found for all cognitive domains suggesting that long-term benzodiazepine users were significantly impaired, compared with controls, in all of the areas that were assessed. However, this study has several limitations, one being that it includes a relatively small number of studies.
    • Barker et al, (2004), CNS Drugs, 18(1) 37-48
    BENZODIAZEPINE AND COGNITION
  • 71.
    • The effects of benzodiazepines on cognition.
    • Neuroimaging studies have found transient changes in the brain after benzodiazepine administration but no brain abnormalities in patients treated long term with benzodiazepines.
    • Such findings suggest that patients should be advised of potential cognitive effects when treated long term with benzodiazepines, although they should also be informed that the impact of such effects may be insignificant in the daily functioning of most patients.
    • Stewart SA (2005) J Clin Psychiatry, 66 Suppl 2: 9-13
    BENZODIAZEPINE AND COGNITION
  • 72.
    • Benzodiazepine use, abuse, and dependence.
    • It is important to distinguish between addiction to and normal physical dependence on benzodiazepines.
    • Few cases of addiction arise from legitimate use of benzodiazepines.
    • Pharmacologic dependence, a predictable and natural adaptation of a body system long accustomed to the presence of a drug, may occur in patients taking therapeutic doses of benzodiazepines.
    • Due to the chronic nature of anxiety, long-term low-dose benzodiazepine treatment may be necessary for some patients; this continuation of treatment should not be considered abuse or addiction.
    • O'brien CP. (2005)J Clin Psychiatry,66 Suppl 2:28-33.
    BENZODIAZEPINE DEPENDENCE
  • 73.
    • Assessing the risks and benefits of benzodiazepines for anxiety
    • disorders in patients with a history of substance dependence.
    • There is much ambiguity over appropriate definitions for benzodiazepine abuse and dependence
    • Furthermore, benzodiazepines do not appear to induce relapse of substance abuse in these patients.
    • The position that benzodiazepines are contraindicated in former substance abusers appears to lack empirical justification.
    • Benzodiazepines may be indicated in certain patients with anxiety disorders and a history of substance abuse or dependence.
    • Posternak MA (2001) Am J Addict, 10(1):48-68.
    • The presence or absence of a history of alcohol use disorders is not a strong predictor of the use of benzodiazepines in subjects with anxiety disorders over 12 months of prospective follow-up.
    • Mueller TI (1996) J Clin Psychiatry, 57(2):83-9.
    BENZODIAZEPINE DEPENDENCE
  • 74.
    • In 1990, the APA task force on BZD’s concluded that BZD are not drugs of abuse though it is common among people actively abusing alcohol, opiates, sedative hypnotics.
    • Selzman C (1991) Am. J Psychiatry, 148:151-52
    • In early 1980’s studies indicated that long term administration of BZD at therapeutic doses produce physical dependence. So in 1990’s it was recommended that these agents should (esp. short t 1/2 ) be tapered gradually when discontinuing them
    • Rosenbaum JR (2005) J. Clin. Psychiatry, 66 Suppl 2: 4-8
    • By 1999 International group of experts recommended the use of BZD for anxiety disorders even for long periods
    • Uhlenhuth EH (1999) J Clin. Psychopharmacol, 19 (6): 23S-29S
    BENZODIAZEPINE DEPENDENCE
  • 75.
    • Retrospective analysis of hypnotic overdose in 1989-90 found a decrease in BZD overdose and a statistically significant rise in non BZD sedative overdose
    • Hofman RS (1991) NY State J Med, 91:436-439
    • BZD are less toxic in overdose than alternatives, are safe, and have little liability for abuse among patients without history of abuse
    • Rosenbaum JR (2005) J. Clin. Psychiatry, 66 Suppl 2: 4-8
    BENZODIAZEPINE OVERDOSE CHANGING ATTITUDE TO BZD
  • 76.
    • Don’t we have antipsychotics that produce cognitive dysfunction
    • Don’t we have antidepressants that produce cognitive dysfunction
    • Doesn’t anxiety produce cognitive dysfunction
    • Don’t we read about cognitive dysfunction in schizophrenia and bipolar
    • Haven’t we heard of withdrawal of antipsychotics, antidepressants and anticonvulsants
    CRITIQUE
  • 77.
    • Is it not therefore a question of
      • Rational/irrational use ?
      • Use/misuse/abuse ?
      • Combinations that are useful and dirty?
      • And what of useful and dirty combinations in neurobiology
    CRITIQUE
  • 78.
    • Are we aware of what we are talking about?
    ISSUE 5
  • 79.
    • BZDs allosterically modulate GABA neurotransmission by potentiating GABA’s ability to increase conductance of chloride through its channel
    BASICS
  • 80.
    • 19 different sub units grouped into 5 classes according to the degree of amino acid identity
    • Alpha 1-6, Beta 1-3, gamma1-3,Delta, Theta, epsilon, pi and Rho1-3
    • Alpha subunits, especially 1 ,2 and 5 are important for receptor activation by GABA
    • Most GABA A receptor complexes are α 1 β 2 γ 2
    • Specifically α and γ subunits are thought to determine GABA A-BZD receptor pharmacology
    GABA RECEPTOR
  • 81.
    • BDZ1 (Omega - 1) -preferentially labelled by triazolopyridazines, imidazolopyridine and pyrazoloqinolines. Also, beta carbolines.
    • BDZ1 rich areas - lamina IV of cerebral cortex, cingulate cortex , globus pallidus, nucleus basalis, substantia nigra pars reticulata, molecular layer of the cerebellum, Amygdaloid nucleus , periaqueductal gray matter, ventral pallidum and inferior colliculus.
    • Implicated in sleep wakefulness mechanism
    BENZODIAZEPINE RECEPTOR
  • 82. BZD-2 receptors (Omega-2) - caudate putamen, olfactory bulb, cerebral cortex, hippocampus and dentategyrus Related to cognitive, memory and psychomotor function. BZD-3(Omega-3) are not directly associated with GABA receptors or with chloride channels . They may regulate the synthesis of neuroactive steroids. BENZODIAZEPINE RECEPTOR
  • 83. BDZ GABA Cl Channel GABA BENZODIAZEPINE RECEPTOR
  • 84.
    •  1 – Sedative, amnestic, ataxic and partly anticovulsant
    •  2 and 3 – Anxiolytic
    •  3 – DA system receives GABAergic inhibitory input
    •  5 – Cognitive
    •  3 – Immobilisation action of propofol and etomidate.
    •  2 - Hypnotic and respiratory depression
    • GABA A receptor subtype selective anxiolytics
      • L-838417
      • SL 651498 (Full agonist at  2 and  3, partial agonist at  1 and 5)
      • GLB139-  3 selective BZ agonist
    GABA RECEPTOR - SELECTIVITY Whiting PJ (2006) Curr Opinion Pharmacol 6: 24-29 Rudolf U & Mohler H (2006) Curr Opinion Pharmacol, 6:18-23
  • 85. GABA RECEPTOR
  • 86. GABAergic System Morris B et al (2005) Current Opinion in Pharmacology 5 : 101 - 106  2 CCK/VIP+  1
  • 87. GABAergic System
  • 88.
    • Prescribing is not carefree but requires monitoring to obtain optimal risk benefit ratio
    • Benzodiazepines are therefore ‘GOOD’ and are here to stay
    ISSUE 6 BALANCING THE OPTIONS
  • 89.
    • So Benzodiazepine is a friend not a foe
    • However it is maybe an evil albeit necessary if not rationally prescribed
    CONCLUSION
  • 90.
    • “ Apply your breaks”
    CONCLUSION Don’t blame the machine If the driver is at fault
  • 91. The most deserving six-letter word....... “ THANKS" for your patient listening.