Alcoholism


Definition: Alcoholism -> continued abuse of beverages containing ethyl alcohol that lead to damage and disturbance to the subject and his environment.
Chronic alcoholism -> set of changes in somatic and psychic productts chronic abuse of that substance.
The alcoholic personality: neurotic psychopathic structures, abnormal impulsive individuals, iperemotivi, anxious, insecure, passive.
Sex-work: higher incidence in males; family situation: economic misery, social deficiency, work frustration, poor education, lack of affection, low cultural level, especially housewives now thwarted.
Damage social disintegration nucleus, accidents, road accidents, somatic diseases concomitanti.Esiste an interrelationship between the individual [use-abuse of alcohol] - Environment:
Individual genetics, personality, family, work habits ;-->[ alcohol use, abuse, dependency] -> environment: culture, religion, law, economics.



. DEPENDENCE FROM 'ALCOHOL.
Biochemical basis.
In February 1970 Davis and Waish Veterans Administration Hospital Baylor (USA) formulate a hypothesis on the mechanisms of action of alcohol on the CNS: a correlation existed between the metabolism of the opiates and alcohol, some intermediate alkaloids benziliso -quinoline of Papaver somniferum, were like other alkaloids, the TIQ tetrahydroquinolinium or intermediary metabolism of alcohol.
Hypothesis of the link between alcohol and opioids (hypotesis LINK):
dopamine in the CNS and also degrades in the first aldehyde and then acid dopamine dopamine;
Alcohol is metabolized into acetaldehyde and then to CO2 and H2O by the acetaldehyde dehydrogenase;
aldehyde dopamine competes with acetaldehyde, acetaldehyde dehydrogenase aldehyde leads to excessive production of dopamine;
dopamine excess aldehyde is combined with molecules of dopamine formed TIQ (tetra hydro papaveroline) that resemble morphine.
Ethanol, acetaldehyde and TIQ seem to bind preferentially to one or more receptors for the opioid delta.
It is therefore now believe that these alkaloids morphine-like play a key role in preparing the craving and alcohol dependence.
So even there on alcohol as a common mechanism opioids biochemist and a circuit located in brain areas (s.limbico, n.accumbens, globus pallidus), which is responsible place of compulsive behavior towards these substances.
.. Cascade theory of reward.
In areas of the brain reward occurs following interactions:
serotonin in the hypothalamus activates the opioid receptors and causes release of enkephalins in the ventral tegmental nucleus. The enkephalins inhibit GABA in the substantia nigra.
The GABA B receptor level inhibits and controls the amount of dopamine that is released in the ventral tegmental area of the nucleus and acts in the nucleus accumbens. Stimulation of rec. GABA b implies a reduction in the amount of dopamine released from the nucleus accumbens and thus less activation of dopamine D2 receptors result is a leveling down of the sense of gratification.
The release of dopamine also depends enkephalins GABAergic pathways;
dopamine in the amygdala may also be issued;
In terms of the A6 of the locus ceruleus noradrenergic system exists connected with the gratification with fibers projecting all'ipoccampo. GABA receptors in the hippocampus to determine noraadrenalina issue.
SUMMARY.
For the cascade theory of alcoholism is seen that the chronic abuse of alcohol leads to:
Reduced levels of serotonin in the hypothalamus;
Increased levels of hypothalamic enkephalins
increase of GABA in the nucleus accumbens
reduced level of dopamine in the nucleus accumbens.
Alcohol and neuroregolazione.
Effects on meurotrasmettitori:
Acute administration: the increase GABA on dopamine (nucleus accumbens) increase, the increase Noraepinefrina on 5HT?;
Chronic administration: reduction of GABA on DA reduction, or reduction, the reduction in 5HT;
Alcohol causes a reduction of norepinephrine and dopamine in the brain by reducing the excitatory effects of these substances on the CNS.



. Acute exposure to alcohol leads to inhibition of NMDA receptors with changes in load distribution of Na + and Cl-, inhibiting the function of chloride channels.
The chronic abuse of ethanol affects the appearance of functional adaptations to compensate for the progressive decrease of receptor dell'NMDA, caused by the ability to inhibit alcohol. Consequent increase in the number of NMDA receptors in cerebellum and hippocampus. Abrupt withdrawal of alcohol unlock the receptors and causes sudden entry of Ca + + resulting in the phenomenon of hyperarousal and convulsion. Resulting hyperactivity of glutamatergic synapses and excitotoxicity.
The chronic abuse of alcohol leads to an increase of GABA in the CNS. GABA receptors are divided into GABA A and GABA B, the former are widely distributed in the CNS and are associated with an ion channel for chloride, with membrane hyperpolarization and inhibition of NMDA receptors and thus a reduction of excitation. The GABA B are less well represented and have an encoder system connected all'adenilato cyclase.
ACUTE ALCOHOL EFFECTS
GABA A receptor will reinforce current Chlorine with inhibition of nerve transmission;
Chronic Effects
Down regulation of GABA A and reduction in number, with reduction of inhibitory transmission and sensitivity of GABAergic alcohol.
Chronic exposure causes an increased release of noraadrenalina deposits from central and peripheral (CNS and adrenal gland).
Cholinergic system: Inhibition of choline uptake by reducing the concentration of acetylcholine and consequent dementia alcohol to reduced activity of choline-acetyltransferase.
Serotonin: alcohol enhances the transmission on the rec. 5HT3 and activates the dopamine system.
Endogenous opioids: these alcohol increases met-enkephalin and beta-endorphins in acute. In chronic reduces levels of endorphins.
Interaction with s.dopaminergico: mesh medial forebrain (MFB) in the hypothalamus is responsible for the positive reinforcement that is associated with the use of substances, namely the satisfaction or pleasure derived from the use of alcohol or drugs. The MFB has 4 areas: lateral hypothalamus, ventral tegmental area or VTA, nucleus accumbens and frontal cortex or ACC.
The 'Belly tegmental area is home to the gratification for alcohol and opiates.
The nucleus accumbens is linked to VentroTegmentale via dopaminergic pathways. Alcohol acts on the VTA via the path of TIQ, teraidrochinoline and acts on the cascade of gratification.
Alcohol dependency
This explains the mechanism for positive reinforcement, or the gratification that give the alcohol and the negative reinforcement mechanism: the fear of abstinence
The release of dopamine is blocked by opioid antagonists, naltrexone. It is believed that the release of dopamine in n.accumbens is mediated by beta endorphin and delta agonists and miu.
ASPECTS OF S. Neuropsychiatric ADDICTION TO ALCOHOL.
Into acute and chronic
ACUTE: 1) alcoholic intoxication, 2) idiosyncratic alcohol intoxication, 3) uncomplicated alcohol withdrawal, 4) delirium from alcohol withdrawal.
a) Acute alcohol intoxication: recent ingestion of alcohol that cause intoxication in most subjects: 1) appearance of adaptive changes in behavior, 2) at least one physical sign and 3) exclusion of any other disorder;
Diagram alcohol:
100-200 mg% = neurological signs: ataxia, s. cerebellar s. vestibular s. psychic.
> 300 mg% = coma or comatose state, hypothermia.
- Clinical picture of acute
Step 1: change of mood, hypomania, more rarely, depression, impulsivity, aggression, lack of criticism, impaired affect, road accidents, work accidents, trauma, suicide (for change of mood);
Phase 2 = motor incoordination, dysarthria, diploopia, ataxia, = benign prognosis, evolution ominous rare.
b) idiosyncratic intoxication: is a rare event, occurs in individuals for amounts of alcohol intake less than most other individuals are susceptible. S *: a history of the disorder, no clinical characteristic behavioral disturbances (psychomotor excitement, characteristics reactions).
c) uncomplicated alcohol withdrawal
First hand tremors, nausea and vomiting, sweating, mild (in the first 24 hours) then under suspension from complete after 24 hours -> insomnia, headache, anxiety, dysphoria, depression, ipereattivitą of SNA with tachycardia, sweating, hypertension, mild disorientation in time, withdrawing in 5-7 days residual insomnia and irritability.
d) delirium from alcohol withdrawal or delirium tremens. Prodrome: anxiety, restlessness, insomnia, nightmares, with visions of terrifying, low-grade fever. Acute delirium with disorders of consciousness (a state of dream-like confusion); perception disorders with hallucinations and / or illusions zooptiche visual, tactile, olfactory, acoustic cobinate.
Thought disorder with attentive defects, memory impairment of fixation, professional delusions, confabulations, or false memories, mental disorder that develops within the context of memory impairment. The mood is "galgenhumor" or gallows humor, mixed with fear, restlessness, anxiety disguised as an environment friendly, playful, teasing and bullying. Polypnoea, tachycardia, hypotension, tremors to great shocks, dysarthria. Mortality of 5% for cardiac arrhythmias, digestive bleeding, infectious complications is the most serious acute framework.
CHRONIC PAINTINGS: 1) alcoholic hallucinosis; 2) anamnestic alcohol disorder, 3) delusions of jealousy 5) alcoholic dementia.
a) Alcoholic hallucinosis: a disorder of perception is essentially without alteration of consciousness, according Kraeplin "hallucinatory madness drinkers" within 48 hours after discontinuation of alcohol the person has the feeling of warning whistles, noises, words, threats, accusations, words sentencing (auditory and visual hallucinations), mood impairment with marked anxiety.
b) anamnestic alcohol disorder or Korsakoff psychosis, Wernicke's encephalopathy complicated by disorder of the function mnesic with retro-anterograde amnesia and confabulation.
c) delusions of jealousy; Ey distinguished three groups of chronic alcoholics in delusional psychoses:
1) delirium of interpretation
2) hallucinatory delusions
3) paranoid delusion
The delusion of jealousy is a clinical picture of chronic course characterized by systematized delusions, uncontrollable, polished, experienced with affective deprivation in the absence of other psychotic and affective acceptance of the idea of posting pseudoadulterio, delirious with lack of recognition of paternity certainty, it aggressively developing suicidal behavior.
Dementia associated with alcoholism.
Impairment of short-term memory and long-term deficits of abstract thinking, ethical and social decay; association with previous delirium tremens, sind. Wernicke-Korsakoff.
Nell'etilismo neurological syndromes.
S. withdrawal -> delirium tremens and alcoholic epilepsy, alcoholic epilepsy: friendly or disease of the ancient Romans for partial or total cessation of alcohol. For metabolic interactions, epilepsy aggravated by alcohol, trauma with cranial hematoma, generalized seizures, tonic-clonic seizures, was wrong;
Jimjams
S.carenziali secondary s. Wernicke alcoholic polyneuropathy or in 5-10% of alcoholics with axonal degeneration and myelin sheath, loss of sensation, numbness, muscle cramps, steppante gait, muscle atrophy, anesthesia for painful compression of the logs muscle;
-Deficiency optic neuropathy with reduct. vision, difficulty reading and color recognition, scotomas;
-Alcoholic cerebellar degeneration with ataxia, tremor.
Therapy of acute: control of respiratory depression, acid-base balance, blood volume, blood glucose, metadoxil ev acting sull'ADH; vitamins in chronic forms, thiamine;
delusions of jealousy neuroleptics, haloperidol, thioridazine.
Delirium tremens: cardiotonic, steroids, benzodiazepines, hydro-saline balance correction;
individual and group psychotherapy.
THERAPY cessation.
Disulfiram or Antabuse perlongetten (drug history) or Antabuse, which inhibits the conversion of acetaldehyde into acetate accumulation with the first.
S. is hired for a week then comes the test of the glass; scheme: disulfiram 400 mg capsules dose increasing to two cps / day
Antidepressants: SSRIs: fluoxetine, venlafaxine, citalopram, paroxetine). Usually use of serotonin reuptake inhibitors
Gamma hydroxybutyric acid (Alcover): 5-8 ml three times in the evening to increase the dosage of 2-3 ml. Inhibits an increase in dopamine in the striatum and increases levels of acetylcholine, reducing the activity of NMDA receptors sensitive to excitatory neurotransmitters (glutamate and aspartate) binding to GABA B (5-10 ml x 3 times daily)
Naltrexone: why prevent alcohol may lead to pleasure through the release of dopamine from the nucleus accumbens antagonize the action of TIQ oppiodomimetica ventro tegmental area.

dott.Claudio Mario Italiano
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