<p></p><div>Addiction
research has largely targeted regions of the ventral striatum (the nucleus
accumbens core and shell), as well as the dopamine-releasing neurons of the
ventral mesencephalon. The ventral mesencephalon (i.e.
midbrain) densely innervate the nucleus accumbens.&nbsp;<span style="font-size: 1rem;">Activation
of the dopaminergic innervation of the nucleus accumbens (termed the mesolimbic
dopamine system) is the neuronal substrate for the rewarding or reinforcing
properties of drugs of abuse (Roberts et al. 1980; Di Chiara and Imperato
1988; Wise 1989, 1996; Kuhar et
al. 1991; Koob
1992; Fibiger et al. 1992; Dworkin and Smith 1993; Schulteis
and Koob
1996; White 1996).</span></div><img src="@@PLUGINFILE@@/Nucleus%20Accumbens.png" alt="Nucleus Accumbens" width="400" height="293" class="img-responsive atto_image_button_left"><br><p></p><p>In short, t<span style="font-size: 1rem;">he
release of dopamine from the mesolimbic pathway into the nucleus accumbens
regulates&nbsp;</span><span style="background-color: rgb(255, 255, 255); font-size: 1rem;">incentive salience</span><span style="font-size: 1rem;">&nbsp;(e.g.
motivation and desire for&nbsp;</span><span style="background-color: rgb(255, 255, 255); font-size: 1rem;">rewarding stimuli</span><span style="font-size: 1rem;">)
and facilitates&nbsp;</span><span style="background-color: rgb(255, 255, 255); font-size: 1rem;">reinforcement</span><span style="font-size: 1rem;">&nbsp;and
reward-related motor function learning.&nbsp;</span>The
dysregulation of the mesolimbic pathway and its output neurons in the nucleus
accumbens plays a significant role in the development and maintenance of
an&nbsp;addiction.</p><h3><br></h3><h3><br></h3><h3><br></h3><h3>Crack / Cocaine</h3><p></p><div>Alper, et al., (1990) determined: “The
major QEEG finding was increased absolute and relative alpha power” in crack
cocaine users.&nbsp;<span style="font-size: 1rem;">Prichep,
et al (2002) discovered in 57 male users, two
major subtypes:</span></div>

<div>◦1)
an alpha cluster characterized by significant deficits of low frequency
activity (&lt;8Hz), significant excess of alpha activity (8-12Hz) and
relatively more normal levels of beta activity; and </div>

<div>◦2)
a beta cluster characterized by deficits of delta, normal amounts of theta and
anterior excess of alpha and beta activity. (Prichep et al., 2002).&nbsp;</div><br><p></p><h3>Stimulants</h3><p></p><div>Stimulants increase the activity in the Reticular Activating System, with the Raphe
nucleus releasing norepinephrine,
decreasing the polarization in the reticular nucleus of the thalamus, and thus increasing the “clocking” or peak frequency
of the rhythmic alpha activity and increasing faster activity.<br></div><br><p></p><p><img src="@@PLUGINFILE@@/Reticular%20Activating%20System.png" alt="Reticular Activating System" width="600" height="341" class="atto_image_button_middle"></p><div>Both&nbsp;Dextrostat and Adderal&nbsp;are similar in
effect, with&nbsp;<u>decreased slower activity </u>and <u>increased beta </u>from 12-26 Hz. There is a paradoxical
increase in alpha noted in the QEEG (Itil et al., 1980). </div>

<div><br></div><div>Methylphenidate:&nbsp;Ritalin&nbsp;produces
a <u>decrease in delta and theta</u>,
with a more pronounced <u>posterior
alpha increase and an increase in low beta</u>, with effects delayed up to 6 hours,
compared to the rapid effects of the amphetamines.</div><h3>Methamphetamines</h3><p></p><div>Methamphetamine dependent volunteers with 4 days of abstinence had
increased EEG power in the delta and theta bands.&nbsp;&nbsp;<span style="font-size: 1rem;">Within the methamphetamine dependent group, a majority of the conventional EEGs were
abnormal (64%), compared to 18% in the non-methamphetamine using group (Newton
et al., 2003).&nbsp;</span><span style="font-size: 1rem;">Methamphetamine exposure is associated with long-lasting reductions in
markers for dopaminergic neurons.</span></div><div><span style="font-size: 1rem;"><br></span></div><h3></h3><h3>Alcohol</h3><div><span style="font-size: 1rem;"><div>Acute
alcohol increases dopamine release across the striatum primarily due to
increased firing of midbrain dopaminergic neurons.</div>

<div>With alcoholism, tolerance
develops, and more alcohol is consumed.&nbsp;<span style="font-size: 1rem;">Concomitantly,
adaptations in glutamatergic, GABAergic, and dopamine transmission occur and
greater or continued amounts of alcohol can result in allostatic changes to
preserve normal brain function. This allostasis is characterized by aberrant
glutamate, GABA, and opioid signaling, as
well as, a dysfunction in nigrostriatal
and mesolimbic dopamine transmission.</span></div><img src="@@PLUGINFILE@@/Ventral%20Striatum.png" alt="Ventral Striatum" width="500" height="423" class="img-responsive atto_image_button_middle"><p></p><ul><li>Alcohol consumption is the third
largest risk factor for poor health (<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4106030/">WHO, 2011</a>)</li><li>One profile
that has a predisposition to alcohol: Low voltage</li><li>Low Voltage
EEG can be due to excessive GABAA receptor sites</li></ul></span></div><p><img src="@@PLUGINFILE@@/Low%20Voltage%20EEG.png" alt="Low Voltage EEG" width="605" height="537" class="img-responsive atto_image_button_left"><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><h3>Cannabis / Hashish / THC&nbsp;</h3><p></p><div><span style="font-size: 1rem;">Marijuana and its sister drugs will:</span><br><ul><li>Increase
frontal alpha amplitude, </li><li>increased
frontal coherence across the hemispheres</li><li>Increased
phase synchrony (hypo phase lag).&nbsp; These findings are reported in chronic
exposures.</li><li>Effects on dampening reaction times
in evoked potentials have been noted as well</li></ul></div>







Regular
use of cannabis over many years lowers levels of dopamine, a key chemical in
the brain’s reward center. <br>The dopamine system is central to learning and motivation. We conclude that
long-term cannabis use in people is linked to blunting of the dopamine
system.<br><p></p><p><img src="@@PLUGINFILE@@/Dopamine.png" alt="Dopamine" width="400" height="366" class="img-responsive atto_image_button_text-bottom"><br></p>