Benzodiazepines and Anxiety

overmedicated-pharmaby Jen L’Insalata

Benzodiazepines, sometimes referred to as anti-anxiety medications, are intended for the use in treating severe rehabilitating panic attacks and panic disorder. However all too often, benzodiazepines are prescribed for generalized anxiety disorder. From a biological etiology, anxiety is the result of stimuli triggers that activate a series on neurochemical and hormonal responses that prepare the body and mind for immediate activation. This sequence is commonly referred to as the fight or flight response and the limbic system and amygdala become activated. The excitatory hormones cortisol, adrenaline, and norepinephrine are released and the locus coeruleus or gated chloride ion channels are excited (Preston, O’Neal, & Talaga, 2013).

Generalized anxiety disorder is the low level chronic stress experienced throughout an individual’s life. This differs from panic attack in that there is a persisting anticipation of stressful or dangerous events. The limbic system is kept on a lower level of alert but does not cross the threshold into full activation of the fight or flight response.

Panic disorder is characterized by a series of reoccurring panic attack which may appear to be unprovoked. There is strong evidence suggesting the biological etiology of panic attacks stem from hypersensitive neurons within the limbic system, specifically when concerning GABA (Preston, O’Neal, & Talaga, 2013).  This causes individuals to experience dizziness, nausea, chest palpitations, shortness of breath, and profuse sweating that accompany and intense fear.

Benzodiazepines bind to chloride ion channels enhancing the flow of negative chloride ions. This inward flow of negatively charged chloride ions decreases neuron excitation and produces a calming effect on the brain. Benzodiazepines work by interacting with benzodiazepine receptors during presynaptic inhibition. By binding with the receptor sites, the calming effects of the influx of negative chloride ions as well as the effects of GABA are enhanced (Preston, O’Neal, & Talaga, 2013).

The first Benzodiazepine, chloriazepoxide was developed in 1957 for anxiety and insomnia. Since then several other forms of the drug have been developed with varying degrees of anti-anxiety and hypnotic properties. Benzodiazepine gained popularity in pharmisudical anxiety treatment due to its rapid effectiveness. Therapeutic effects can be experienced in as little as 30 minutes. Additionally, benzodiazepines are well tolerated by most individuals (Preston, O’Neal, & Talaga, 2013).

Although considered relatively non-addictive, I have seen numerous cases of benzodiazepine abuse while working with addictions. Many individuals utilizes benzodiazepine to escape unwanted generalized anxiety symptoms and do not have adequate coping skills. Such coping skills can be developed through psychotherapeutic means.

I have observed the use of benzodiazepines to alleviate anxiety cause by other drugs, withdrawal, and the lack of healthy coping skills. Many individuals use benzodiazepines as an intermediary drug or for relaxation purposes. I often observe the illicit use of benzodiazepine coupled with various forms of opiates, a combination that can often be fatal.

For this reason, I question and caution the frequent and over use of benzodiazepines as a primary pharmaceutical treatment for anxiety. As they are effective to reduce dehabilitating anxiety quickly, this medication should be reserved for panic attacks and panic disorder. If prescribed, the duration should be limited and quantity should begin at a low dosage.

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References

Preston, J. D., O’Neal, J. H., & Talaga, M. C. (2013). Handbook of clinical psychopharmacology for therapists (7th ed.). Oakland, CA: New Harbinger. ISBN: 9781608826643.

A Brief Overview of Neurons and Neurotransmission

neuronsJen L’Insalata

Preston, O’Neal, & Talaga (2013), presented the comparison of neural transmission to a telephone switchboard. In many ways, that analogy is accurate since neurotransmitters are essentially messages being sent from one nerve to another. Neurons utilize electrical and chemical stimulation to communicate and ultimately control human behavior.

To understand how transmissions are passed between neural pathways, one must first understand the basic structure of a nerve cell. The main body of the nerve cell or neuron is known as the soma. Its shape differs depending on its specific function but is contains the structures universal to all cells such as the nucleus, mitochondria, and cytoplasm. The axon is a slender tube like structure that emanates from the soma. It is often covered by a myelin sheath which aids in the conduction of information from one neuron to another; known as an action potential. Terminal buttons are the end points of axons which secrete hormones known as neurotransmitters. To do this an action potential must travel down the axon and reach the terminal buttons. The neurotransmitter either excites or inhibits the action potential allowing it to continue or cease its communication with the neighboring neuron. The dendrites of the neighboring neuron receive the transmission from the terminal button across a fluid filled gap called a synapse. The dendrite resembles the branches of a tree and allow the transmission to continue along the neural pathway (Carlson, 2014. & Saladin, 2012).

 

Neural transmission and action potentials are governed by the balance of positively and negatively charged ions such as sodium, potassium, and chloride. Polarization of the intracellular fluid by salutatory conduction and diffusions allows the transmission of the action potential down the length of the axon until it reaches the terminal buttons. If the action potential is strong enough at the terminal button, synaptic vesicles containing neurotransmitters are able to bind with the presynaptic membrane of the terminal button. This membrane essentially separates the end of the terminal button from the synaptic cleft. The synaptic vesicle is then able to release the neurotransmitter across the intracellular fluid which fills the gap, or synapse, between the terminal button and the opposing dendrite (Carlson, 2014. & Saladin, 2012).

 

Neurotransmitters are transported from the cell body to the terminal button by sac-like structures called vesicles. The vesicles bind to the membrane of the terminal button ans create tiny opening from which the neurotransmitter is released from the presynaptic neuron. Neurotransmitters are then ale to cross they synapse and bind with receptors on the dendrites of the postsynaptic neuron facilitating communication. While some neurotransmitters bind with the receptor sites on the post synaptic neuron, others are destroyed, or reabsorbed by the terminal button of the presynaptic neuron (Reed, Carlson, Quale, 2016).

 

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Resources

Carlson, N. R. (2014). Foundations of behavioral neuroscience (9th ed.). Boston, MA: Pearson. ISBN: 9780205940240.

Preston, J. D., O’Neal, J. H., & Talaga, M. C. (2013). Handbook of clinical psychopharmacology for therapists (7th ed.). Oakland, CA: New Harbinger. ISBN: 9781608826643.

Reed, L., Carlson, L, Quale, S. (2016). Capella University Neurotransmission Retrieved from http://media.capella.edu/course media/PSY7330/animation/transcript.htm1

Saladin. K.S. (2012). Anatomy and Physiology: The Unity of Form and Function. 6th ed. Mcgraw-Hill. New York, NY. ISBN978-0-07-337825-1.